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NTRODUCTION Type 2 diabetes is sometimes called a “life style” disease

as it more common in people who don’t do enough exercise, have an
unhealthy diet and obese. Type 2 Diabetes was previously seen mainly
in older adults, however it is becoming more common in young children due
to obesity and overweight children.

3. HISTORY The earliest known record of diabetes was written on 3rd Dynasty
Egyptian papyrus by physician ‘Hesy-Ra’. He stated recurring urination
as a sign of this illness

4. HISTORY The Indian physician Sushruta in the 6th century B.C. noticed
the sweet nature of urine in such patients and termed the condition
MADHUMEHA.

5. Diabetes mellitus Greek word "diabainein" meaning "to siphon or pass

through" Latin word "mellitus" meaning "sweetened with honey" "to pass
through sweetened with honey"

6. DIABETIC MELLITUS Diabetes is a group of metabolic diseases

characterized by hyperglycemia resulting from defects in insulin
secretion, insulin action, or both.

7. EPIDEMIOLOGY Globally 382 million people had diabetes in 2013 By 2035,

this number will rise to 592 million In India 65.1 million people had
diabetes in 2013 By 2035, this number will increase by 70.6%

8. Courtesy: 2015 International Diabetes Federation Epidemiology

9. ANATOMY OF PANCREAS The adult pancreas is a transversely oriented

retroperitoneal organ extending from the "C " loop of the duodenum to the
hilum of the spleen EXOCRINE secretion pancreatic juice enzymes promote
the digestion of carbohydrates, proteins and fats ENDOCRINE secretion
Insulin and glucagon- enter portal vein – transported directly to the
liver – regulate metabolism of carbohydrates, proteins and fats.
10. PANCREAS 15- 20% α cells synthesize and secrete GLUCAGON 70-
80% β cells synthesize and secrete INSULIN 1-8% δ cells synthesize
and secrete STOMATOSTATIN and GASTRIN 1-2% F- cells secrete PANCREATIC
POLYPEPTIDE which decreases the absorption of food from the GIT

11. INSULIN Polypeptide hormone produced by β- cells of islets of

Langerhans of pancreas Insulin is a protein made of 2 chains- alpha
and beta Anabolic hormone STRUCTURE OF INSULIN

12. REGULATION OF INSULIN SECRETION Factors stimulating insulin

secretion : Glucose: The effect is more predominant when glucose is
administered orally. Arise in blood glucose level is a signal for insulin
secretion. amino acids: gastrointestinal hormones: Gastrointestinal
hormones (secretin, gastrin) enhance the secretion of insulin.

13. REGULATION OF INSULIN SECRETION Factors inhibiting insulin

secretion • Epinephrine is the most potent inhibitor of insulin release.
• In emergency situations like stress, extreme exercise and trauma, the
nervous system stimulates adrenal medulla to release epinephrine. •
Epinephrine suppresses insulin release and promotes energy metabolism by
Mobilizing energy-yielding compounds-glucose from liver and fatty acids
from adipose tissue

14. Gluconeogenesis : The synthesis of glucose from non- carbohydrate

precursors( e.g. amino acids, glycerol) Glycogenesis: The formation of
glycogen from glucose. Glycogenolysis : The breakdown of glycogen to
glucose

15. ACTIONS OF INSULIN Stimulation of the activity of glycolytic enzymes

Reduces the activity of the enzymes of gluconeogenesis Increased
synthesis of glycogen Increased uptake of of glucose by resting skeletal
muscles Reduction of blood glucose level Reduction of lipolysis and
stimulation of lipid synthesis

16. INSULIN Pancreas secretes 40-50 units of insulin daily in two steps:
• Secreted at low levels during fasting ( basal insulin secretion •
Increased levels after eating (prandial) • An early burst of insulin
occurs within 10 minutes of eating • Then proceeds with increasing release
as long as hyperglycemia is present

17. GLUCOSE HOMEOSTASIS

18. CLASSIFICATION Classification by American diabetic association

2009 : • Type 1 diabetes • Type 2 diabetes • Gestational diabetes mellitus
(GDM) • Secondary DM: Hormonal problems, pancreatic disorders, drugs
19. TYPE 1 DM Juvenile / IDDM (5 to 10%) Autoimmune destruction of
pancreatic beta cells. Individual has an absolute insulin deficiency
and no longer produces insulin. Such patients are absolutely dependent
on exogenously administered insulin for survival.

20. TYPE 2 DIABETES MELLITUS

21. TYPE 2 DM Most common type Comprises 90 to 95% of DM cases

Most type 2 DM patients are overweight, and most are diagnosed as adults.
Approximately half of the patients are unaware of their disease

22. Peripheral resistance to insulin, especially in muscle cells

Increased production of glucose by the liver Insulin secretary defect of
the beta cells • Obesity contributes greatly to insulin resistance •
Insulin resistance generally decreases with weight loss TYPE 2 DM The
underlying pathophysiologic defect in type 2 DM is characterized by the
following three disorders:

23. COMPONENTS OF DM-II Type 2 diabetes Insulin resistance -cell

dysfunction

24. RISK FACTORS NON-MODIFIABLE: Age: 45 or more Race : African

American, Asian American, Hispanic or Latino. Familial history : a
parent, or siblings with diabetes.

25. RISK FACTORS MODIFIABLE: Pre diabetes Heart and blood disease
Hypertension Low HDL cholesterol and high triglycerides. Obesity
Polycystic ovary syndrome Physical inactivity

26. RESEARCH INPUT High Bone Mineral Density and Fracture Risk in Type
2 Diabetes as Skeletal Complications of Inadequate Glucose Control.
Ling Oei, Abbas, Karol Estrada et al Journal : Diabetes Care 2013 Jun;
36(6) Objective: To examine the influence of glucose control on skeletal
complications.

27. RESEARCH INPUT RESEARCH DESIGN AND METHODS: prospective

population-based study 420 participants with type 2 diabetes were
classified by glucose control - according to HbA1c adequately
controlled diabetes (ACD: n = 203; HbA1c <7.5%) inadequately controlled
diabetes (ICD; n = 217; HbA1c≥7.5%) no diabetes (n = 3,715)

28. RESEARCH INPUT RESULTS : The ICD group had 1.1–5.6% higher BMD,
and 1.2 to −1.8% narrower femoral necks than ACD and ND, respectively.
Participants with ICD had 47–62% higher fracture risk than individuals
without diabetes whereas those with ACD had a risk similar to those without
diabetes. CONCLUSIONS : Poor glycemic control in type 2 diabetes is
associated with fracture risk.

29. CLINICAL PRESENTATION Patients can be asymptomatic Polyuria

Polydipsia Polyphagia Fatigue Weight loss Most patients are
discovered while performing urine glucose screening

30. DIAGNOSIS Fasting Plasma Glucose Oral Glucose Tolerance Test

(OGTT) Glycoselated Hemoglobin (HbA1c) Urinalysis • Glycosuria •
Ketone bodies

31. HBA1C •Measures the amount of glycated haemoglobin in blood. •HbA1c

is not sensitive enough to detect DM but is the gold standard for the long
term monitoring.

32. ADDITIONAL INVESTIGATIONS; Lipid profile Fundoscopic examination

LFT , Urine analysis ECG Test to assess other complications

33. Any one test should be confirmed with a second test, most often fasting
plasma glucose (FPG). DIAGNOSTIC CRITERIA • Classic signs of
HYPERGLYSEMIA with CPG ≥200mg/D • OGTT ≥200mg/dL • FPG ≥126mg/dL • A1C
≥ 6.5%

34. “WHO” DIAGNOSTIC CRITERIA CONDITION 2 HRS GLUCOSE FASTING GLUCOSE

HbA1C UNIT Mg/dl Mg/dl % Normal <140 <110 <6 Impaired fasting glycemia
<140 110 – 126 6 -6.4 Impaired glucose tolerance >140 <126 6 – 6.4
DM >200 >126 > 6.5

35. MANAGEMENT OF DIABETES MELLITUS

36. The major components of the treatment of diabetes are: MANAGEMENT OF

DM • Medical Nutrition Therapy(Diet and Exercise)A • Oral hypoglycaemic
therapyB • InsulinC

37. Dietary treatment should aim at: Ensuring weight control.

Providing nutritional requirements. Allowing good glycaemic control
with blood glucose levels as close to normal as possible. Correcting
any associated blood lipid abnormalities. A. DIET

38. DIETARY MANAGEMENT DIETARY MANAGEMENT Follow individualized meal

plan and snacks as scheduled Balanced diabetic diet – 50% CHO, 30%
fats, 20% CHON, vitamins and minerals diet based on pts. size, wt.,
age, occupation and activity. Meal should include more fiber and starch
and fewer simple or refined sugars.

39. DIETARY MANAGEMENT If taking insulin, eat extra food before periods
of vigorous exercise Routine blood glucose testing before each meal
and at bedtime is necessary during initial control, during illness and
in unstable pts. Excessive salt intake is to be avoided. It should be
particularly restricted in people with hypertension and those with
nephropathy

40. Eat grains in the least processed state possible. Limit potatoes
and refined grain products. Avoid concentrated sweets (jellies, jams,
cakes, ice cream) Choose foods with healthy fats. Have 3 meals and
one or two snacks each day Eat slowly and stop when full. Avoid periods
of fasting and feasting, Do not skip meals How to eat low GI food

41. Physical activity promotes weight reduction and improves insulin

sensitivity, thus lowering blood glucose levels. Exercise same time
and duration of day. People should, however, be educated about the
potential risk of hypoglycaemia and how to avoid it. Avoid during poor
metabolic control. Avoid trauma to extremities. EXERCISE

42. EXERCISE PRECAUTIONS Patients who have BS >250mg/dl and who have
urine ketones should not begin exercise until urine tests are NEGATIVE.
Use of proper footwear. Avoid exercise in extreme heat or cold
Have snacks after the exercise , to avoid post exercise hypoglycemia.

43. There are currently four classes of oral anti-diabetic agents: i.

Biguanides ii. Insulin Secretagogues – Sulphonylureas iii. Insulin
Secretagogues – Non-sulphonylureas iv. α-glucosidase inhibitors v.
Thiazolidinediones (TZDs) vi. DPP4i B. ORAL ANTI-DIABETIC AGENTS

44. MAJOR CLASSES • Body to insulin +/- control hepatic glucose production
• Stimulate the pancreas to make more insulin • Slow the absorption of
starches Thiazolidinediones Biguanides Sulfonylureas Meglitinides
Alpha-glucosidase inhibitors

45. Oral Anti-diabetic Agents

46. BIGUANIDES Metformin : is the only drug of this class presently

available in market It does not cause hypoglycaemia MOA : They
increase glucose uptake and utilisation in skeletal muscle (thereby
reducing insulin resistance) and reduce hepatic glucose production
(gluconeogenesis). Pharmacokinetic : Metformin has a half-life of about
3 hours and is excreted unchanged in the urine.

47. METFORMIN Side effects : -Dose-related gastrointestinal

disturbances -lactic acidosis is a rare but potentially fatal toxic effect
-Long-term use may interfere with absorption of vitamin B12 Contra
indications: • Renal failure • Hepatic disease • Hypoxic pulmonary disease
• Heart failure or shock Temporarily discontinued before any radiographic
procedure involving intravenous iodinated contrast, as patients are at
an increased risk of lactic acidosis.

48. INSULIN SECRETAGOGUES SULFONYLUREAS : Inhibit KATP Channel of ß-cells

First-generation agents Tolbutamide Acetohexamide Tolazamide
Chlorpropamide Second-generation Glipizide Glyburide Glimepiride

49. SULFONYLUREAS Hypoglycemia is the most common and most serious

adverse event associated with SU therapy Weight gain, regarded as a
class effect of Su’s Contraindicaton: liver failure, renal failure
patients. Most sulfonylureas cross the placenta and enter breast milk;
as a result, use of sulfonylureas is contraindicated in pregnancy and in
breast feeding P’kinetics : Orally given, Some is oxidised in the liver
to moderately active products and is excreted in urine; 50% is excreted
unchanged in the faeces.

50. NON-SULFONYLUREA SECRETAGOGUES MEGLITINIDES • MOA: Inhibit KATP

Channel of ß-cells • Very fast onset of action, rapidly metabolized by
liver enzymes, with a peak effect within 1 hour, the duration of action
is 5–8 hr. • Short duration of action and a low risk of hypoglycaemia
• Medications in this Class: repaglinide ,nateglinide

51. THIAZOLIDINEDIONES ↓ Insulin resistance by making muscle and

adipose cells more sensitive to insulin. They also suppress hepatic
glucose production. Side effects: weight gain, oedema, Hypoglycemia
(if taken with insulin) Contraindication: patients with abnormal LFT
or CHF Medications in this class: pioglitazone , rosiglitazone,

52. Α-GLUCOSIDASE INHIBITORS Acarbose : An inhibitor of intestinal

α-glucosidase. MOA : It delays carbohydrate absorption, reducing the
postprandial increase in blood glucose . Unwanted effects : flatulence,
loose stools or diarrhoea, and abdominal pain and bloating. Like
metformin, it is helpful in obese type 2 patients, and it can be
co-administered with metformin.

53. TREATMENT OF TYPE 2 DIABETES Diagnosis Therapeutic Lifestyle Change

Combination Therapy - Oral Drug with Insulin Combination Therapy - Oral
Drugs Only Monotherapy

54. If glycaemic control is not achieved (HbA1c > 6.5%) with lifestyle
modification within 1 –3 months, ORAL ANTI-DIABETIC AGENT should be
initiated. In the presence of marked hyperglycaemia in newly diagnosed
symptomatic type 2 diabetes (HbA1c > 8%, FPG > 11.1 mmol/L), oral
anti-diabetic agents can be considered at the outset together with
lifestyle modification. MONOTHERAPY

55. Combination oral agents is indicated in: Newly diagnosed

symptomatic patients with HbA1c >10 Patients who are not reaching
targets after 3 months on monotherapy COMBINATION ORAL AGENTS

56. DIABETES MANAGEMENT ALGORITHM

57. Short-term use: Acute illness, surgery, stress and emergencies

Pregnancy Breast-feeding Insulin may be used as initial therapy in
type 2 diabetes Severe metabolic decompensation (diabetic ketoacidosis,
hyperosmolar nonketotic coma, lactic acidosis, severe
hypertriglyceridaemia). INSULIN THERAPY

58. Long-term use: If targets have not been reached after optimal dose
of combination therapy, consider change to multi-dose insulin therapy.
INSULIN THERAPY

59. INSULIN INJECTION SITES

60. ROUTES OF ADMINISTRATION Subcutaneous for long term regular use

Intravenous infusion in acute conditions- diabetes Ketoacidosis,
Perioperative period, Hyperosmolar Nonketotic state ONLY NEUTRAL/ CLEAR
INSULIN CAN BE USED Intraperitoneal – Peritoneal dialysis patients
Inhaled insulin- experimental

61. COMPLICATIONS OF INSULIN THERAPY Hypoglycemia Lipodystrophy

Systemic allergic reactions Insulin resistence Dawn phenomenon
Somagyi's phenomenon

62. METHODS OF INSULIN THERAPY Insulin syringe: Insulin pens Jet

injectors Insulin Pumps

63. PATIENT EDUCATION Taking care of diabetes will help to reduce blood
glucose, blood pressure, and cholesterol levels in target ranges.
Caring for your diabetes can also help prevent other health problems over
the years. Follow your healthy eating plan every day. Be physically
active every day. Take your medicines every day. Check your blood
glucose levels every day.

64. COMPLICATIONS OF DIABETES

65. COMPLICATIONS OF DIABETES MELLITUS I. Acute complications: diabetic

ketoacidosis hypoglycemia diabetic nonketotic hyperosmolar coma II.
Chronic complications: a. Microvascular retinopathy nephropathy
 neuropathy diabetic foot dermopathy b. Macrovascular
Cerbro-vascular. Cardio-vascular. peripheral vascular disease.

66. HYPOGLYCEMIA Hypoglycemia is the most frequent acute complication

in diabetes. Signs and symptoms are most common when blood glucose
levels fall <60 mg/dL CAUSE: Missing meals or excessive exercise
Alterations or errors in insulin dosage Alcohol ingestion

67. CLINICAL MANIFESTATIONS OF HYPOGLYCEMIA: Autonomic dysfunctions:

1. Hunger 2. Tremor 3. Palpitation 4. Anxiety 5. Pallor 6. Sweating
Neurologic dysfunctions: 1. Impaired thinking 2. Change of mood 3.
Irritability 4. Headache 5. Convulsion 6. Coma

68. MANAGEMENT MILD (Self treated) Oral fast acting carbohydrate (10-
15gm) – taken as glucose drink or candy Severe :(semi conscious or
comatose patient) IV hypertonic glucose 25% or 50% concentration
Glucagons injection- i.m Glucagon (1mg)

69. DIABETIC KETOACIDOSIS - It is a true emergency - CAUSES: Omitting

insulin in type 1 DM or increase insulin requirements, Infection
Trauma Myocardial Infarction Stroke Surgery Emotional stress
Mortality rate is around 5%.

70. CLINICAL PRESENTATION

71. MANAGEMENT Fluid replacement: 0.9% NaCl IV Insulin therapy for

hyperglycemia: To restore the metabolic abnormalities. Titrate the dose
according to the blood glucose level. • 50U insulin in 50 ml NS iv via
infusion pump 6U/hr initially 3U/hr when blood glucose < 270mg/dl
2U/hr when blood glucose < 180mg/dl Electrolyte correction.
Acidosis correction. Treatment of precipitating cause.

72. HYPERGLYCEMIA HYPEROSMOLAR NONKETONIC SYNDROME (HHNK) Occurs when

there is insufficient insulin to prevent hyperglycemia, but there is
enough insulin to prevent Ketoacidosis Occurs in all types of diabetes,
Esp Diabetes Type 2 Life threatening medical emergency Characterized
by : Plasma osmolarity 340 mOsm/L or greater normal: 280 -300) Blood
glucose severely elevated, 600 - 1000 or 2000 (normal 70- 110)
Undetectable ketonuria and Absence of acidosis

73. HHNKS Major difference from diabetic ketoacidosis is the lack of

ketonuria because there is some residual ability to secrete insulin in
NIDDM. CLINICAL MANIFESTATION: Altered level of consciousness
(lethargy to coma) Neurological deficits: hyperthermia, motor and
sensory impairment, seizures Dehydration: dry skin and mucous membranes,
extreme thirst.

74. MACRO-VASCULAR COMPLICATIONS Ischemic heart diseases.

Cerebrovascular diseases. Peripheral vascular diseases. Diabetic
patients have a 2 to 6 times higher risk for development of these
complications than the general population

75. HYPERTENSION IN DM Mostly present at diagnosis Affects about 60%

of patients Secondary to insulin resistance Increases risk for
retinopathy, nephropathy Dyslipidaemia in DM Most common abnormality
is HDL and Triglycerides A low HDL is the most constant predictor
of Cardiovascular disease in DM.

76. PERIPHERAL VASCULAR DISEASE Increased risk for Types 1 and 2

diabetics. Development of arterial occlusion and thrombosis resulting
in gangrene. Gangrene from diabetes is themost common cause of non-
traumatic lower limb amputation

77. SCREENING FOR MACROVASCULAR COMPLICATIONS 1. Examine pulses for

cardiovascular diseases. 2. Lipid profile. 3. ECG. 4. Blood pressure.

78. Microvascular complications are specific to longstanding

hyperglycaemia. Both Type1 DM and Type2 DM are susceptible to
microvascular complications. The duration of diabetes and the quality
of diabetic control are important determinants of microvascular
abnormalities. MICROVASCULAR COMPLICATIONS

79. DIABETIC RETINOPATHY Affects 60 % of Type 2 diabetics progressive,

irreversible vision loss. Damage to the tiny blood vessels that supply
the eye • Micro aneurysms • Scattered exudates • Cotton wool spots (<5)
• Venous dilatations NORMAL RETINA Cotton wool spots

80. DIABETIC NEPHROPATHY (DN) Diabetic nephropathy is defined by

persistent albuminuria (>300 mg/day), decrease glomerular filtration
rate and rising blood pressure. About 20 – 30% of patients with diabetes
develop diabetic nephropathy - Manifested as: - Microalbuminuria -
Progressive diabetic nephropathy leading to end-stage renal disease

81. TREATMENT TO PREVENT PROGRESSION TO DN All diabetic patients should

be screened annually for microalbuminurea. Tight glycemic control and
management of the blood pressure ACE-inhibitors are recommended to
decrease the progression of nephropathy Smoking cessation. Proteins
restriction. Lipid reduction.
82. DIABETIC NEUROPATHY Damage to the Nerves due to hyperglycemia
Types of Neuropathies… Sensory-Motor Polyneuropathy • Numbness,
paresthesias. • Feet are mostly affected, hands are seldom affected. •
Complicated by ulceration (painless), charcot arthropathy • Decreased
deep tendon reflexes

83. DIABETIC NEUROPATHY Autonomic neuropathy Can affect almost any

system - Manifested by orthostatic hypotension, diabetic diarrhea,
erectile dysfunction, and difficulty in urination.

84. RESEARCH INPUT Effect of mechanical vibration on transcutaneous

oxygen levels in the feet of type 2 diabetes mellitus patients. Núñez
Carrera L, Alessi Montero A ,et al Journal of clinical medicine: 2016
Nov 18. objective : To determine whether whole body vibration favors
some parameters of interest related to complications associated with the
diabetic foot syndrome.(Transcutaneous oxygen levels (TcPO2)>40mmHg in
cases of diabetic foot syndrome are associated with a good prognosis in
the resolution of ulcers.)

85. METHOD:54 patients with DM were included in a 12-week exercise

program based on whole body vibration. Glycemic control was determined
on the basis of the patients' levels of (HbA1c); sensitivity and TcPO2
levels of each foot were also recorded. RESULTS: A significant 7mmHg
increase was observed in the concentration of TcPO2. CONCLUSION: Whole
body vibration may increase TcPO2 levels with useful implications for the
prevention or management of complications associated with restricted
blood perfusion in the diabetic foot syndrome.

86. NURSING MANAGEMENT

87. NURSING ASSESSMENT Obtain history : it includes, Current problems

and General health history Family history Has the patient experienced
polyuria,polydipsia, polyphagia, and any other symptoms? Number of
years since diagnosis of DM? Symptoms of complications?

88. NURSING ASSESSMENT PHYSICAL EXAMINATION: General: Recent wt. loss

or gain, fatigue, anxiety Skin: lesion, infections, dehydration, Eyes:
changes in vision, “floaters, halos, cataracts… Cardiovascular:
orthostatic hypotension, claudication GI: diarrhea, increased hunger
and thirst GU: polyurea, nocturia Neurologic: numbness, and tingling
of extremities

89. 1.Imbalanced nutrition : more than body requirement related to intake

of excess of activity expenditures. • Assess the current timings and
content of meals • Advise patient on the importance of an individualized
meal plan in meeting weight loss goals. • Explain the importance of
exercise in maintain / reducing body weight. • Assist the patient to
establish goals for weekly weight loss and incentives to assist in
achieving them.

90. Risk for injury ( hypoglycemia) related to effects of insulin,

inability to eat. • Closely monitor blood glucose levels to detect
hypoglycemia. • Instruct the patient in the importance of accuracy in
insulin preparation and meal timings to avoid hypoglycemia. • Treat
hypoglycemia promptly with 15 to 20 gm of fast acting carbohydrates. •
Encourage patients to carry sugar candy all times. • Encourage patient
to wear identification bracelet

91. • Assess level of knowledge of disease and ability to care self. •

Assess adherence to diet therapy, monitoring procedures, medication,
treatment, and exercise regimen. • Assess for signs for hyperglycemia or
hypoglycemia. • Perform skin and extremity assessment for peripheral
neuropathy or any injury in feet and lower extremities. Deficit knowledge
related to use of oral hypoglycemic agents

92. Assess feet and legs for skin temperature sensation, soft tissue
injures, corn, dryness, hammer toe, Maintain skin integrity by
protecting feet from break down. Use heel protectors, special
mattresses, foot cradles for patient on bed rest. Avoid Appling drying
agent to skin. (alcohol) Apply moisturizers to maintain suppleness and
prevent cracking and fissures. Instruct patient in foot care guidelines
Risk for impaired skin integrity related to decreased sensation and
circulation to lower extremities.

93. FOOT CARE Patient should check feet daily Wash feet daily Keep
toe nails short Protect feet Always wear shoes Look inside shoes
before putting them on Always wear socks Break in new shoes gradually

94. Discuss with the patient the perceived effect of diabetes on

lifestyle, finances, family life, occupation. Explore previous coping
strategies and skills that have had positive effects. Encourage patient
and family participation in DM self care regimen Assist family in
providing emotional support. Ineffective coping related to chronic
disease and complex self care regimen.

95. SPECIAL PATIENT POPULATION 1. Adolescent Type 2 DM - Type 2 DM is

increasing in adolescent - Lifestyle modification is essential in these
patients - If lifestyle modification alone is not effective, metformin
the only labeled oral agent for use in children (10-16 years)
96. CONCLUSION Type 2 diabetes is a “life style” disease,
characterized by hyperglycemia resulting from defects in insulin
secretion, insulin action, or both. Caring for diabetes can also help
prevent other health problems over the years.

roblems of the vascular system includes disorders of the arteries and

veins. Peripheral arterial disease is a term used to describe a wide
variety of conditions affecting arteries in the neck, abdomen and
extremities. Peripheral arterial disease can be subdivided into
occlusive disease, aneurismal disease, and vasopastic phenomenon. In
contrast,venous diseases primarily affect the lower extremities and can
be categorised into venous thrombosis and chronic venous insufficiency.

3. DEFINITION • Pulmonary embolism is the blockage of pulmonary arteries

by thrombus,fat or air emboli and tumour tissue. • It is the most common
complication in hospitalised patients. • An embolus is a clot or plug that
is carried by the bloodstream from its point of origin to a smaller blood
vessel, where it obstructs circulation.

4. INCIDENCE • Actual incidence of mortality and morbidity from pulmonary

embolism is unknown, it is estimated that nearly 50,000 people die of
pulmonary disease each year in the United states and another 650,000 have
non fatal pulmonary embolism.

5. ETIOLOGY AND RISK FACTORS • Virtually all pulmonary embolisms develop

from thrombi(clots),most of which originate in the deep
calf,femoral,popliteal,or iliac veins. • Other sources of emboli include
tumours, fat, air, bone marrow, amniotic fluid, septic thrombi, and
vegetations on heart valves that develop with endocarditis. • Major
operations ,especially hip, knee, abdominal and extensive pelvic
procedures predispose the client to thrombus formation because of reduced
flow of blood through pelvis. • Travelling in cramped quarters for a long
time or sitting for long periods is also associated with stasis and
clotting of blood.

6. • The most common sources of embolism are proximal leg deep venous
thrombosis (DVTs) or pelvic vein thromboses. • Any risk factor for DVT
also increases the risk that the venous clot will dislodge and migrate
to the lung circulation, which may happen in as many as 15% of all DVTs.
• The conditions are generally regarded as a continuum termed venous
thromboembolism (VTE). • The development of thrombosis is classically due
to a group of causes named Virchow's triad (alterations in blood flow,
factors in the vessel wall and factors affecting the properties of the
blood). • Often, more than one risk factor is present.

7. • Alterations in blood flow: immobilization (after surgery, injury,

pregnancy (also procoagulant), obesity (also procoagulant), cancer (also
procoagulant) • Factors in the vessel wall: surgery, catheterizations
causing direct injury ("endothelial injury") • Factors affecting the
properties of the blood (procoagulant state): – Estrogen-containing
hormonal contraception – Genetic thrombophilia (factor V Leiden,
prothrombin mutation G20210A, protein C deficiency, protein S deficiency,
antithrombindeficiency, hyperhomocysteinemia and
plasminogen/fibrinolysis disorders) – Acquired thrombophilia
(antiphospholipid syndrome, nephrotic syndrome, paroxysmal nocturnal
hemoglobinuria) – Cancer (due to secretion of pro-coagulants)

8. CLINICAL FEATURES • Severity of clinical manifestations of pulmonary

embolism depends on the size of the emboli and the size and number of blood
vessels occluded.Most common manifestations are, Anxiety Sudden
onset of unexplained dyspnea Tachypnea or tachycardia Cough
Pleuritic chest pain Hemoptysis Crackles

9. Fever Accentuation of the pulmonic heart sound Sudden change in

mental status as a result of hypoxemia •In massive emboli, Shock Pallor
Severe dyspnea Crushing chest pain Pulse is rapid and weak Bp is
low ECG indicates right ventricular strain

10. •In medium sized emboli, Pleuritic chest pain Dyspnea Slight
fever Productive cough with blood streaked sputum •In small emboli,
Pulmonary hypertension ECG and chest X-ray indicates right ventricular
hypertrophy

11. PATHOPHYSIOLOGY • When emboli travel to the lungs, they lodge in the
pulmonary vasculature . • The size and number of emboli determine the
location. • Blood flow is obstructed ,leading to decreased perfusion of
the section of the lung supplied by the vessel. • The client continues
to ventilate the lung portion ,but because the tissue is not perfused,
resulting in hypoxemia.

12. •If an embolus lodges in a large pulmonary vessel, it increases

proximal pulmonary vascular resistance, causes atelectasis, and
eventually reduces cardiac output. •If the embolus is in a smaller vessel,
less dramatic clinical manifestations follow but perfusion is still
altered. •The arterioles constrict because of platelet degranulation,
accompanied by a release of histamine, serotonin, catecholamines and
prostaglandins. •These hemical agents result in bronchial and pulmonary
artery constriction. •This vasoconstriction probably plays a major role
in the hemodynamic instability that follows pulmonary embolism.

13. •Pulmonary embolism can lead to right sided heart failure. •Once the
clot lodges, affected blood vessels in the lung collapse. •This collapse
increases the pressure in the pulmonary vasculature. •The increased
pressure increases the work load of the right side of the heart, leading
to failure. •Massive pulmonary embolism of the pulmonary artery can also
result in cardiopulmonary collapse from lack of perfusion and resulting
hypoxia and acidosis.

14. DIAGNOSTIC STUDIES History and physical examination Venous

studies Chest X-ray Continous ECG monitoring ABGs CBC count
with WBC differential D –dimer level Lung scan(ventilation and
perfusion) Pulmonary angiography Spiral CT scan

15. MEDICAL MANAGEMENT • The objectives of treatment are, Prevent

further growth or multiplication of thrombi in the lower extremities
Prevent embolization from the upper or lower extremities to the pulmonary
vascular system. Provide cardiopulmonary support if indicated.

16. CONSERVATIVE THERAPY • The administration of O2 by mask or cannula

may be adequate for some patients.O2 is given in a concentration
determined by ABG analysis. • In some situations,endotracheal intubation
and mechanical ventilation may be needed to maintain adequate oxygenation.
• Respiratory measures such as turning, coughing and deep breathing are
necessary to prevent or treat atelectasis.

17. •If shock is present, vasopressor agents may be necessary to support

systemic circulation .If heart failure is present, digitalis and
diuretics are used. •Pain resulting from pleural irritation or reduced
coronary blood flow is treated with narcotics, usually morphine.

18. DRUG THERAPY • Anticoagulant therapy-Properly managed anticoagulant

therapy is effective in the treatment of many patients with pulmonary
embolism. • Heparin and Warfarin are the anticoagulant drugs of choice.
• Unless contraindicated, heparin should be started immediately and is
continued while oral anticoagulants are initiated. • The dosage of heparin
is adjusted according to PTT and warfarin dose is determined by
International normalized ratio.

19. •Fibrinolytic therapy-The effectiveness of fibrinolytic therapy in

the management of a massive pulmonary embolism is not clear,but it may
be useful in clients who are hemodynamically unstable. •Thrombolytic
agents lyse the clots and restore right- sided heart function.

20. SURGICAL MANAGEMENT • Surgical interventions that may be used in the

treatment of pulmonary embolism include, Vena caval interruption with
the insertion of a filter and Pulmonary embolectomy • The Greenfield
filter, a basket like cone of wires bent to look like an umbrella ,is the
most commonly used filter.

21. •The filter is inserted by threading it up the veins in the leg or

neck until it reaches the venacava at the level of renal arteries. •The
filter allows blood flow while trapping emboli, however venacava filters
are less effective than coagulation and may lead to deep vein thrombosis
and so these are generally are used only when anticoagulants are
contraindicated or ineffective.

22. •Embolectomy is used in clients with significant hemodynamic

instability caused by the embolus,especially those with unstable
circulation and contraindications to thrombolytic therapy. •An
embolectomy involves surgical removal of emboli from the pulmonary
arteries by either thoracotomy or an embolectomy catheter.

23. CONCLUSION • Lower airway disorders include asthma, chronic air flow
limitations and inflammations of the airways. • Nursing care centers on
reversal of any airway spasm and education of the client about how to live
with the disorder and how to reduce the risk of future problems. •
Pulmonary embolism is a potentially life threatening disorder that
usually can be managed effectively with prompt recognition.

Pulmonary Embolism – The Killer Clot in the Lungs • Pulmonary embolism

(PE) is a common and potentially lethal condition. • Most patients who
succumb to PE do so within the first few hours of the event. •The most
important conceptual advance regarding PE is the realization that
pulmonary embolism is not a disease; rather, it is a complication of venous
thrombo-embolism (VTE), most commonly deep venous thrombosis (DVT).

3. Definition Pulmonary embolus (PE) refers to obstruction of the

pulmonary artery or one of its branches by material (eg, thrombus, tumor,
air, or fat) that originated elsewhere in the body. •Originate primarily
from deep venous system of lower extremities •Ilio-femoral thrombi and
pelvic veins appear to be the most clinically recognized •Air, amniotic
fluid and fat emboli are rarer causes.
4. Why care? • PE is the most common preventable cause of death in
hospitalized patients. ~600,000 deaths/year • 80% of pulmonary emboli
occur without prior warning signs or symptoms • 2/3 of deaths due to
pulmonary emboli occur within 30 minutes of embolization • Death due to
massive PE is often immediate

5. Incidence • 2nd most common cause of unexpected death in most age groups.
• Present in 60-80% of patients with DVT, more than 50 % them are
asymptomatic • Account for 15 % of all postoperative deaths • It is
estimated that in the USA .100 000 people die each year of pulmonary
embolism

6. Incidence •A mortality rate up to 30% if untreated due to recurrent

embolization and 2-8 % mortality if well treated. •The overall incidence
is higher in males compared with females (56 versus 48 per 100,000,
respectively. However, the incidence rises with increasing age,
particularly in women after the age of 75 years .

7. PE Indian Scenario : PGIMER, Chandigarh study An autopsy study on 1000

medical patients at the Postgraduate Institute of Medical Education and
Research (PGIMER), Chandigarh revealed- PE was present in 159 (16%) of
1000 patients who died hospital — 1. It was a fatal embolus in 36 2. A
major contributor to death in 90 patients 3. 30 patients, the embolus was
an incidental finding at autopsy as death occurred due to some other cause.
THE NATIONALMEDICAL JOURNAL OF INDIA VOL. 23, NO.4, 2010

8. Normal anatomy of the lung and its circulation

9. PE can arise from anywhere in the body, most commonly it arises from
the calf veins. The venous thrombi predominately originate in venous valve
pockets and at other sites of presumed venous stasis.

10. Rudolf Virchow Rudolf Virchow postulated more than a century ago that
a triad of factors predisposed to venous thrombosis. Rudolph Virchow, 1858
Triad: Hypercoagulability Stasis to flow Vessel injury

11. RISK FACTORS Modifiable Risk Factors for Venous Thromboembolism •

Obesity • Metabolic syndrome • Cigarette smoking • Hypertension • Abnormal
lipid profile • High consumption of red meat and low consumption of fish,
fruits, and vegetables

12. RISK FACTORS Non Modifiable : Advancing age Personal or family history
of VTE Congestive heart failure (So in AHF , prophylaxis is indicated)
Chronic obstructive pulmonary disease Acute infection, Air pollution
Postmenopausal hormone replacement therapy
13. Air travel and risk of PE The risk of fatal PE in this setting is less
than 1 in 1 million. •Activation of the coagulation system during air
travel. •For each 2-hour increase in travel duration, there appears to
be an 18% higher risk of VTE.

14. ETIOLOGY •Nearly all PEs arise from thrombi in the lower extremity
or pelvic veins (deep venous thrombosis [DVT]). •Risk of embolization is
higher with thrombi proximal to the calf veins. •Thromboemboli can also
originate in upper extremity veins

15. PATHOPHYSIOLOGY

16. Pathophysiology There are both respiratory and hemodynamic

consequences associated with pulmonary embolism.

17. Pathophysiology - Respiratory consequences It include the following:

•Increased alveolar dead space •Hypoxemia •Hyperventilation

18. •Vascular obstruction of pulmonary artery •Ventilation without

perfusion = increase alveolar dead space = hypoxemia •Bronchoconstriction
and increase airway resistance (due to secretion of vaso and broncho
active substances such as serotonin) •Alveolar hyperventilation due to
reflex stimulation of irritant receptors = hypocapnia Pathophysiology of
PE

19. Hemodynamic Consequences of PE

20. Hemodynamic consequences complete or partial obstruction of a

pulmonary artery alveolar dead space is increased impaired or absent gas
exchange various substances are released from the clot and surrounding
area causing regional blood vessels and bronchioles to constrict

21. CONTD… Increase in pulmonary vascular resistance Increase in

pulmonary arterial pressure Increase in right ventricular work to
maintain pulmonary blood flow Right ventricular failure Decrease in
cardiac output,systemic blood pressure and the development of shock

22. PATHOPHYSIOLOGY Pulmonary artery pressure increases only if more

than 30–50% of the total cross-sectional area of the pulmonary arterial
bed is occluded by thrombo-emboli. PE-induced vasoconstriction,
mediated by the release of thromboxane A2 and serotonin, contributes to
the initial increase in pulmonary vascular resistance after PE

23. PATHOPHYSIOLOGY Anatomical obstruction and vasoconstriction lead to

an increase in pulmonary vascular resistance and a proportional decrease
in arterial compliance. Increase in pulmonary vascular resistance results
in RV dilation, which alters the contractile properties of the RV
myocardium

24. The increase in RV pressure and volume leads to an increase in wall

tension and myocyte stretch. RV contraction time is prolonged, while
neuro-humoral activation leads to inotropic and chronotropic stimulation.
Together with systemic vasoconstriction, these compensatory mechanisms
increase pulmonary artery pressure, improving flow through the obstructed
pulmonary vascular bed, and thus temporarily stabilize systemic blood
pressure (BP). PATHOPHYSIOLOGY

25. The extent of immediate adaptation is limited, since a

non-preconditioned, thin-walled right ventricle. RV is unable to generate
a mean pulmonary artery pressure above 40 mm Hg. Result both of abnormal
RV wall tension and of circulatory shock PATHOPHYSIOLOGY

26. PE - Types

27. 1. Air embolism •An air embolism occurs when one or more air bubbles
enter a vein or artery and block it. •Symptoms of a severe air embolism
might include low blood pressure or difficulty breathing. •Arterial and
venous air embolism •Treatment for an air embolism has three goals: •to
stop the source of the air embolism •to prevent the air embolism from
damaging •to resuscitate (hyperbaric oxygen therapy)

28. 2. Fat embolism •Fat embolism is caused by introduction of fat or bone

marrow particles into the systemic venous system and then into pulmonary
arteries. • Early splinting of fractures of long bones and operative
rather than external fixation are thought to help prevent fat embolism.
•Maintenance of intravascular volume is important because shock can
exacerbate the lung injury

29. 3. Amniotic fluid embolism An amniotic fluid embolism (AFE) is a rare

obstetric emergency in which amniotic fluid, fetal cells, hair, or other
debris enters the mother's blood stream via the placental bed of the uterus
and triggers an allergic-like reaction. There is no specific treatment
for amniotic fluid embolism, and initial emergency management is the same
as for any other cause of sudden maternal collapse( with cardiovascular
and respiratory resuscitation and correction of the coagulopathy.)

30. 4. Septic embolism •A septic embolism is a type of embolism that is

infected with bacteria, resulting in the formation of pus that embolizes
to the lung. •Common microbes that can lead to widespread dissemination
of septic emboli is Fusobacterium necrophorum, a Gram negative anaerobic
bacillus. •Treatment includes that of the underlying infection.
31. 5. Foreign body embolism Foreign body embolism caused by introduction
of particulate matter into the pulmonary arterial system, usually by IV
injection of inorganic substances.

32. 6.Tumor embolism Tumor embolism is a rare complication of cancer

(usually adenocarcinoma) in which neoplastic cells from an organ enter
the systemic venous and pulmonary arterial system, where they lodge,
proliferate, and obstruct flow

33. ACC/AHA Classification Massive Submassive Low-Risk PE

Pulmonary infarction syndrome

34. Massive PE Acute PE with sustained hypotension (systolic bp 90 mm Hg

for at least 15 min. or requiring inotropic support, not due to a cause
other than PE, such as •Arrhythmia •Hypovolemia •Sepsis •Left ventricular
(LV) dysfunction •Persistent profound bradycardia (heart rate 40 bpm with
signs or symptoms of shock)

35. Saddle Embolus • Clot occurs at the point of the pulmonary artery
branching. •It can be fatal, due to the large amount of blood flow is
inhibited.

36. Submassive PE Acute PE without systemic hypotension but with either

RV dysfunction or myocardial necrosis Angiographically defined blockage
of flow to an area served by less than two lobar arteries. These patients
have acute or unexplained dyspnea with exertion or at rest.

37. Sub massive PE RV dysfunction means the presence of at least 1 of the

following • RV dilation or RV systolic dysfunction on echocardiography
• Elevation of BNP (90 pg/mL) • Electrocardiographic changes (new complete
or incomplete RBBB, anteroseptal ST elevation or depression, or
anteroseptal T wave inversion)

38. Low-Risk PE Acute PE and the absence of the clinical markers of adverse
prognosis that define massive or submassive PE

39. Pulmonary Infarction Syndrome Caused by a tiny peripheral pulmonary

embolism • Pleuritic chest pain, often not responsive to narcotics •
Low-grade fever • Leukocytosis • Pleural rub • Occasional scant hemoptysis

40. Clinical Features •Size of the embolus and blood vessel Occluded.
•State of the lung. •Associated disease(s).

41. Presentation •Dyspnea at rest (73 %) •Pleuritic pain (44 %) •Cough

(34 %) •Orthopnea (28 %) •Calf or thigh pain (44 %) •Wheezing (21 %) Rapid
onset of dyspnea Within seconds (46 %) within minutes (26 %) •
Tachypnea (54 %) • Tachycardia (24 %) • Rales (18 %), • Decreased breath
sounds (17 %) • Jugular venous distension (14%) Most Common Symptoms Most
Common Signs The “classic” signs and symptoms of pulmonary embolism,
namely dyspnea, hemoptysis, and chest pain.

42. Differential Diagnosis

43. Diagnosis Risk stratification Clinical examination Bed side

tests (ECG, ABG, pulse oximetry) Laboratory tests (D-dimer, Cardiac
biomarkers) Imaging techniques (Ultrasound/ Doppler scan, CXR, CTPA,
V/Q scan, Echocardiogram)

44. Risk stratification • Wells score for PE • Modified Geneva score for
PE

45. Wells score The most commonly used method to predict clinical
probability. In 1995, Philip Steven Wells, developed , to predict the
likelihood of PE, based on clinical criteria. The prediction rule was
revised in 1998, further revised when simplified during a validation by
Wells et al. in 2000.

46. Simplified Geneva Score

47. Diagnosis… Pulmonary Embolism Rule-out Criteria (PERC): Help assess

people in whom pulmonary embolism is suspected. People in this low risk
category without any of these criteria may undergo no further diagnostic
testing for PE: Hypoxia SaO2 <95% Unilateral leg swelling
Hemoptysis, Prior DVT/PE Recent surgery/trauma Age >50 Hormone
use Tachycardia

48. Diagnostic Tests Imaging Studies – CXR – V/Q Scans – Spiral Chest
CT – Pulmonary Angiography – Echocardiograpy Laboratory Analysis – CBC,
ESR, – D-Dimer – ABG’s Ancillary Testing – ECG – Pulse Oximetry

49. D-dimer Test The D-dimer assay is a sensitive but nonspecific test
to detect the presence of venous thromboembolism. •D-dimers are produced
during the degradation of fibrin clot by plasmin (Fibrin split product)
• Circulating half-life of 4-6 hours • Quantitative test have 80-85%
sensitivity False Positives: •Pregnant Patients • Post-partum < 1week
•Malignancy •Surgery within 1 week •Sepsis •Hemorrhage •CVA •Collagen
Vascular Diseases •Hepatic Impairment •Advanced age > 80 years

50. D-dimer Test False Negative D-Dimer – Heparin •A normal D-dimer

result (< or = 500 ng/mL Fibrinogen Equivalent Units{FEU}) has a negative
predictive value. •If the D-dimer reads high, then further testing
(ultrasound of the leg veins or lung scintigraphy or CT scanning) is
required to confirm the presence of thrombus.

51. BNP & pro-BNP •Typically greater in patients with PE. •Sensitivity
of 60% and specificity of 62%. •At a threshold of 500 pg/mL, the
sensitivity of pro- BNP for predicting adverse events was 95%, and the
specificity was 57%.

52. WBC •Poor sensitivity and nonspecific •Can be as high as 20,000 in

some patients Hb •PE does not alter count but if extreme, consider
polycythemia, a known risk factor

53. Pulse oximetry & ABG •Pulse oximetry provides a quick way to assess
oxygenation; hypoxemia is one sign of PE, and it requires further
evaluation. •ABG measurement may show an increased alveolar to arterial
oxygen (A-a) gradient or hypocapnia; one or both of these tests are
moderately sensitive for PE but are not specific. Arterial blood gas
analysis is not diagnostic for pulmonary embolism but typically shows PaO2
less than 80 mm Hg and PaCO2less than 36 mm Hg on room air. physiological
dead space and muscle fatigue then lead to respiratory acidosis.

54. Doppler ultrasound of leg veins Principle - Veins are normally

compressible; Presence of DVT renders veins non-compressible, 50% of
patients with PE have positive ultrasound. (95% of PE are due to leg DVT)

55. ECG 2 Most Common finding on ECG: •Nonspecific ST-segment and T-wave
changes • Sinus Tachycardia •S1Q3T3: Classic signs are a large S wave in
lead I, a large Q wave in lead III, and an inverted T wave in lead III
Acute cor pulmonale or right strain patterns • Tall peaked T-waves in lead
II (P pulmonale) • Right axis deviation • RBBB • S1-Q3-T3 (occurs in only
20% of PE patients)

56. S wave in lead I, a Q wave in lead III, and a T-wave inversion in lead
III. This pattern only occurs in about 10% of people with pulmonary
embolisms

57. Echocardiography This modality generally has limited accuracy in the

diagnosis. •The overall sensitivity and specificity for diagnosis of
central and peripheral pulmonary embolism by ECHO is 59% and 77%. •It may
allow diagnosis of other conditions that may be confused with pulmonary
embolism.

58. Echocardiography Disturbed RV ejection pattern or on depressed

contractility of the RV free wall compared with the RV apex (‘McConnell
sign’)- Reported to retain a high positive predictive value for PE, even
in the presence of pre-existing cardiorespiratory disease. •
Inter-ventricular septal flattening and paradoxical motion toward the LV
resulting in a “D-shaped” LV in cross section. •Tricuspid regurgitation

59. Echocardiography

60. Chest x-ray A normal or nearly normal chest x-ray Major chest
radiographic abnormalities are uncommon.

61. Radiographic signs of acute pulmonary embolism Signs with relative

high specificity but low sensitivity for acute pulmonary embolism:
•Decreased vascularity in the peripheral lung (Westermark sign).
•Enlarged right descending pulmonary artery (Palla's sign) • Pleural
based areas of increased opacity (Hampton hump). •Hemi-diaphragm
elevation

62. Westermark’s sign •Dilation of the pulmonary arteries proximal to

the embolus and the collapse of the distal vasculature. • Represents a
focus of oligemia (hypovolemia)

63. Hampton’s hump shallow Dome-shaped opacity in the periphery of the

lung dur to pulmonary infraction

64. Spiral CT •Major advantage of Spiral CT is speed: •Often the patient

can hold their breath for the entire study, reducing motion artifacts.
•Spiral CT is quicker than the equivalent conventional CT permitting the
use of higher resolution acquisitions in the same study time.
•Contraindicated in cases of renal disease. •Sensitive for PE in the
proximal pulmonary arteries, but less so in the distal segments.

65. Computed tomographic pulmonary angiography Multi-detector computed

tomographic (MDCT) angiography with high spatial and temporal resolution
and quality of arterial opacification, CT angiography has become the
method of choice for imaging the pulmonary vasculature in PE. A negative
MDCT is an adequate criterion for excluding PE in patients with a non-high
clinical probability of PE.

66. Lung scintigraphy/ Ventilation/Perfusion Scan - V/Q Scan”

Ventilation–perfusion scintigraphy (V/Q scan) is an established
diagnostic test for suspected PE. Procedure: - Ventilation scan with Xenon
or technetium inhalation -Perfusion scan with Tc99m labeled radioactive
dye infusion, IV injection of technetium (Tc)-99m-labelled macro
aggregated albumin particles which block a small fraction of the pulmonary
capillaries and thereby enable scintigraphic assessment of lung
perfusion.
67. Ventilation/Perfusion Scan - “V/Q Scan” A common modality to image
the lung. • Relatively noninvasive. • In many centers remains the initial
test of choice • Preferred test in pregnant and renal failure patient
•breastfeeding should be discontinued for 24 hours following use of
radiocontrast • A normal ventilation/ perfusion ratio is reported as
0.8:1.

68. VQ scan Technique

69. Ventillation scan Perfusion scan Normal Ventilation, equally

distributed Left UL PE

70. Pulmonary Angiography

71. Pulmonary Angiography The “gold standard” DSA requires less

contrast medium than conventional cineangiography and has excellent
imaging quality for peripheral pulmonary vessels in patients who can hold
their breath; It is less useful for imaging of the main pulmonary
arteries, due to cardiac motion artefacts.

72. Pulmonary Angiography Left-sided pulmonary angiogram showing

extensive filling defects within the left pulmonary artery and its
branches.

73. Imaging in Pregnancy No validated clinical decision rules No consensus

in evidence for diagnostic imaging algorithm Balance- risk of radiation
vs. risk of missed fatal diagnosis or unnecessary anticoagulation MDCT
delivers higher radiation dose to mother but lower dose to fetus than V/Q
scanning Consider low-dose CT-PA or reduced-dose lung scintigraphy

74. Diagnostic Algorithm

75. Imaging – NUT SHELL •Plain chest radiograph – Usually normal and
nonspecific signs. •Radionuclide ventilation-perfusion lung scan –
Excellent negative predictive value. •CT Angiography of the pulmonary
arteries –Quickly becoming method of choice. •Pulmonary angiography –
Gold standard but Invasive

76. MANAGEMENT

77. 87 Emergency management. –Nasal oxygen to relieve hypoxemia,

respiratory distress, and central cyanosis. –Intravenous infusion lines
to administer medications or fluids. –Hypotension is treated by a slow
infusion of dobutamine . –The ECG is monitored continuously for
dysrhythmias which may occur suddenly. – Intravenous diuretics, and
antiarrhythmic agents may be indicated. –Blood is drawn for serum
electrolytes and CBC –Intubation and mechanical ventilation may be
performed based on clinical assessment and arterial blood gas analysis

78. Emergency management. Aggressive volume expansion is of no benefit

and may even worsen RV function by causing mechanical overstretch Modest
(500 mL) fluid challenge may help to increase cardiac index in patients
with PE, low cardiac index, and normal BP. vasopressors is often necessary,
Norepinephrine appears to improve RV function via a direct positive
inotropic effect. It also increases right coronary perfusion.

79. Emergency management. •Dopamine and dobutamine are first-line

inotropic agents for the treatment of PE-related shock. Both agents
increase cardiac output. •Norepinephrine increases both cardiac output
and systemic vascular resistance and may be beneficial as monotherapy or
in combination with dopamine or dobutamine.

80. –. As soon as massive PE is suspected, high-dose unfractionated

heparin should be administered in larger-than-usual doses. Most patients
should receive at least a 10 000-U bolus of heparin, followed by a
continuous intravenous infusion of at least 1250 U/h, with a target
activated partial thromboplastin time (aPTT) of at least 80 seconds
Emergency management.

81. Medical Management •General measures to improve respiratory and

vascular status • Anticoagulation therapy • Thrombolytic therapy •
Surgical intervention

82. GENERAL MANAGEMENT Oxygen therapy is administered to correct the

hypoxemia, relieve the pulmonary vascular vasoconstriction, and reduce
the pulmonary hypertension.

83. Parenteral anticoagulation Immediate anticoagulation can be

achieved with IV UFH, subcutaneous LMWH, or SC fondaparinux. LMWH or
fondaparinux are preferred over UFH for initial anticoagulation in PE,
as they have lower risk of inducing major bleeding and heparin-induced
thrombocytopenia. UFH is recommended for patients in whom primary
reperfusion is considered, as well as for those with serious renal
impairment (creatinine clearance,30 mL/min), or severe obesity.

84. Anticoagulant Therapy Heparin •Heparin augments the activity of

antithrombin III and prevents the conversion of fibrinogen to fibrin.
•5000-10000 Units IV Loading Dose, Then 1000 Units/hr IV infusion drip
• Duration: 7-10 days OR till clinical improvement • Follow up by PTT
(1.5-2.5)
85. LMWH . •It should be used whenever possible for the initial inpatient
treatment of DVT & PE. Outpatient of DVT, and possibly PE ,is safe and
cost-effective for carefully selected patients.

86. Fondaparinux •Anticoagulant pentasaccharide that specifically

inhibits activated factor X •By selectively binding to antithrombin,
fondaparinux potentiates (about 300 times) the neutralization of factor
Xa by antithrombin •Fondaparinux does not cross-react with Heparin
induced antibodies •FDA has approved fondaparinux for initial treatment
of acute PE and acute DVT as a bridge to oral anticoagulation with warfarin

87. Vitamin K antagonists Gold standard’ in oral anticoagulation.

•Warfarin prevents activation of factor II, VII, IX and X. •. •Heparin
is continued for 4–5 days to overlap with warfarin therapy to counter
paradoxical hypercoagulability that occurs with warfarin monotherapy.

88. Vitamin K antagonists Anticoagulation with UFH, LMWH, or

fondaparinux should be continued for at least 5 days and until the (INR)
has been 2.0–3.0 for two consecutive day. Warfarin can be started at
a dose of 10 mg in younger otherwise healthy outpatients, and at a dose
of 5 mg in older patients and in those who are hospitalized.

89. Novel Anticoagulants Promise immediate onset of action and

administration in fixed doses without routine laboratory coagulation
monitoring •These drugs have few drug-drug or drug-food interactions,
making them more “user friendly” •Dabigatran is a direct thrombin
inhibitor •Rivaroxaban is a factor Xa inhibitor •Both are approved in
Canada and Europe for VTE prevention after knee or hip arthroplasty

90. Thrombolytic treatment Thrombolytic treatment of acute PE restores

pulmonary perfusion more rapidly than anticoagulation with UFH alone
Thrombolytic therapy has replaced surgical embolectomy as the treatment
for hemodynamically unstable patients with massive pulmonary embolism
Accelerated regimens administered over 2 hours are preferable to
prolonged infusions of first-generation thrombolytic agents over 12–24
hours.

91. Unfractionated heparin infusion should be stopped during

administration of streptokinase or urokinase; it can be continued during
rtPA infusion. In patients receiving LMWH or fondaparinux at the time that
thrombolysis is initiated, infusion of UFH should be delayed until 12
hours after the last LMWH injection (given twice daily), or until 24 hours
after the last LMWH or fondaparinux injection(given once daily).
92. Thrombolysis Indications: •Massive PE •Sub-massive PE where risk of
bleeding low (in RVD)

93. THROMBOLYTIC THERAPY Dose Schedules in PE 1. Streptokinase (STK) •

I V bolus 250,000 units over 30’ followed by infusion of 100,000 units/hr
for 12-24 hours 2.Recombinant tissue plasminogen activator (rtPA) • IV
bolus of 15 mg in 10’ followed by 85 mg in next 2 hours (total =100 mg)
• To be followed by heparin infusion on completion of TPA

94. THROMBOLYTIC THERAPY Alteplase •Indications: •Documented PE with: –

Persistent hypotension – Syncope with persistent hemodynamic compromise
– Significant hypoxemia – +/- patient with acute right heart strain
•Approved Alteplase regimen is 100mg as a continuous IV infusion, in 2hr.

95. Before After

96. Potential benefits of TLT •More rapid resolution of symptoms (eg,

dyspnea, Chest pain and psychological distress) •Stabilization of
respiratory and cardiovascular function without need for mechanical
ventilation or vasopressor support •Reduction of RV damage •Improved
exercise tolerance •Prevention of PE recurrence •Increased probability
of survival

97. Potential harm •Disabling or fatal hemorrhage including intracerebral

hemorrhage •Increased risk of minor hemorrhage, resulting in prolongation
of hospitalization and need for blood product replacement

98. Use of Heparin Before and After Thrombolysis:

99. IVC filter • Indications: - DVT with massive pulmonary embolus -

Recurrent PE not treatable with anticoagulation - Absolute
contra-indications for anti-coagulation - Chronic thromboembolic
pulmonary hypertension • Not used in: - Patients with free-floating
thrombi in the proximal veins - Patients scheduled for systemic
thrombolysis, surgical embolectomy

100. Complications associated with IVC filter Early complications •

Device malposition (1.3%) • Pneumothorax(0.02%), • Hematoma (0.6%) • Air
embolism (0.2%) • carotid artery puncture (0.04%) • Arteriovenous fistula
Late complications • Recurrent DVT (21%) • IVC thrombosis (2% to 10%),
• IVC penetration (0.3%) • Filter migration (0.3%) • Recurrent PE (2-5%)
•

101. Catheter Embolectomy Interventional catheterization techniques

Another approach is mechanical clot fragmentation and aspiration.
Pulmonary artery balloon dilation and stenting Successful catheter
embolectomy rapidly restores normal blood pressure and decreases
hypoxemia.

102. Surgical Embolectomy When contraindications preclude thrombolysis.

Surgical excision of a right atrial thrombus. Rescue patients whose
condition is refractory to thrombolysis Older case series suggest a
mortality rate between 20% and 30%

103. Massive Pulmonary Embolism – Management •Begin bolus high-dose IV

unfractionated heparin as soon as massive PE is suspected. • Begin
continuous infusion of heparin to achieve a target aPTT of at least 80
sec. •Volume resuscitation with no more than 500 to 1000 mL of
fluid.( Excessive volume resuscitation will worsen right ventricular
failure. • Have a low threshold for administration of vasopressors and
inotropes.

104. Massive Pulmonary Embolism – Management • If thrombolysis is risky,

consider placement of an inferior vena caval filter, catheter embolectomy,
or surgical embolectomy. •Do not use a combination of thrombolysis and
vena caval filter insertion. (The prongs of the filter insert into the
caval wall. Concomitant thrombolysis predisposes to caval wall
Hemorrhage.) •Consider immediate referral to a tertiary care hospital

105. Pulmonary Embolism in Pregnancy Leading cause of death in pregnancy.

DVT and PE are common during all trimesters of pregnancy and for 6-12 weeks
after delivery. Heparin and fibrinolysis are safe in pregnancy. LMWH
can be given throughout their pregnancy Warfarin is contraindicated
Women experiencing a thromboembolic event during pregnancy should
receive therapeutic treatment with UFH or LMWH during pregnancy,

106. Pregnancy & Postpartum •Pregnant women who are in a hypercoagulable

state or who have had previous venous thromboembolism should receive
prophylactic anticoagulation during pregnancy •Anticoagulation may be
restarted with UFH or LMWH 4- 6 hours following vaginal delivery or 6-
12 hours following cesarean delivery. •Anticoagulation continuing for 4-6
weeks postpartum and for a total of at least 6 months.

107. Thrombolysis in pregnancy Streptokinase (and probably other

thrombolytic drugs) does not cross the placenta because of its high
molecular weight. •However in the mother, bleeding is the major side
effect, usually from the genital tract and often severe. incidence of
bleeding is about 8%. • Because of the risk of bleeding, thrombolysis
should not be used routinely in pregnancy. •Should not be used at the time
of delivery unless it appears that the patient is likely to die
108. Malignancy •Four- to sevenfold higher risk of thrombosis compared
with patients without cancer. •Caused by prothrombotic effects of the
tumor and also because of treatment, particularly with surgery, use of
a central venous catheter,and chemotherapy. •~20% of patients presenting
with VTE have active cancer, associated with reduced survival. •Initial
treatment with heparin and warfarin is given in the standard manner.

109. Complications • Instant Death • Chronic pulmonary hypertension •

Respiratory failure • Congestive heart failure • Recurrence

110. PREVENTION BEFORE SURGERY GENERAL SURGERY • Unfractionated heparin

5000 units SC bid or tid or •Enoxaparin 40 mg SC qd or •Dalteparin 2500
or 5000 units SC qd NEURO SURGERY •Unfractionated heparin 5000 units SC
bid or •Enoxaparin 40 mg SC qd and •Graduated compression stockings or
intermittent pneumatic compression

111. Prevention Prevent deep venous thrombosis. • Active leg exercises

•The intermittent pneumatic leg compression device •Use of elastic
compression stockings •Anticoagulant therapy, Low molecular weight
heparin prophylaxis. •Avoid oral contraceptive pill

112. Intermittent pneumatic compression

113. Genetic Blood Tests 25-50% of patients with VTE have an inherited
disorder There are genetic causes of metabolism which may be tested for
Factor V Leiden – causes increased clotting as variant cannot be
inactivated Factor Protein C Deficiency – results in normal cleaving
of Factor Va and Factor VIIIa

114. Prevention while traveling •Drink plenty of fluids. Preven

dehydration, which can contribute to the development of blood clots..
•Take a break from sitting. Move around the airplane cabin once an hour
or so., •Fidget in your seat. Flex your ankles every 15 to 30 minutes.
•Wear support stockings.

115. Prognosis •5 to 10% of symptomatic PEs are fatal within the first
hour of symptoms. •Prognosis depends on the amount of lung that is affected
and on the co-existence of other medical conditions; •chronic
embolisation to the lung can lead to pulmonary hypertension. •Once
anticoagulation is stopped, the risk of a fatal pulmonary embolism is 0.5%
per year

116. NURSING MANAGEMENT

117. NURSING MANAGEMENT Impaired gas exchange related to decreased
perfusion to lung tissues in pulmonary vascular bed by embolus as
manifested by dyspnea, hypoxemia.

118. •Auscultate breath sounds, noting crackles, wheezes. •Administer

supplemental oxygen as indicated. •Look for indication of mechanical
ventillator •Treat underlying causes ( eg- respiratory acidosis) •Monitor
pulse oximetry and report O2 saturation <92%. •Encourage frequent
position changes. •Maintain chair or bed rest in semi-Fowler’s position.
Support arms with pillows. Outcome- Weaning from invasive to non invasive
MV Normal bilateral entry breath sound Normal ABG findings.

119. Potential for decreased cardiac output related to heart failure as

evidenced by increased CVP ,engorged neck veins, pedal edema •Auscultate
apical pulse, assess heart rate, rhythm. •Inspect skin for pallor,
cyanosis. •Monitor urine output, noting decreasing output and
concentrated urine. •Note changes in sensorium: lethargy, confusion,
disorientation, anxiety, and depression. •Encourage rest, semi recumbent
in bed or chair. •Elevate legs, avoiding pressure under knee. Encourage
active and passive exercises. •Administer IV solutions, restricting total
amount as Outcome- Vitals signs are within normal range Intake output
level maintained

120. Pain related to pulmonary embolism as verbalized by the patient

•Asses the nature of the pain •Asses related factors •Provide comfortable
position •Relieve anxiety •Provide psychological support •Administer
oxygen therapy •Administer analgesics

121. Potential for impaired skin integrity RT edema, immobility etc.

•Asses for the presence of related factor •Observe condition of skin;
pressure sore •Implement pressure relieving mattresses • Maintain
functional body alignment •Provide skin care •Encourage adequate
hydration and nutrition •Encourage ambulation if patient is able

122. Potential for bleeding RT anticoagulant/thrombolytic therapy •Asses

signs and symptoms of bleeding •Asses patient for high risk for bleeding
condition like liver disease, kidney disease, severe hypertension
•Monitor PT level •Monitor IV dosage and delivery system to minimize the
risk of over coagulation / under coagulation. •Institute safety
precautions- Pad the side rails •Avoid IM inj.

123. Cont… •Provide gentle oral care •Avoid constipation •Limit physical
manipulation •Compress IV sites for at least 10 min and arterial sites
for 30 min •Draw all laboratory samples through existing line •Send
specimens for cross matching •Don’t give foods rich in vitamin K

124. Anxiety related to threat of death , change in health habits, increase

in respiratory difficulty •Asses the level of anxiety. •Encourage patient
to ventilate feelings of anxiety. •Asses patient’s normal coping
mechanisms •Support previously effective coping mechanisms - Be
empathetic •Provide adequate rest, Organize activities •Decrease sensory
stimulation

125. •The importance of continued warfarin administration for 3 to 6

months to prevent further thrombus development. •Foods high in vitamin
K, such as dark green vegetables and apricots, must be limited during this
time period to prevent decreased warfarin action. •Therapeutic INR value
should be checked . •Not to use warfarin with acetaminophen, nonsteroidal
anti-inflammatory drugs because such combinations can quickly elevate the
INR. •To wear a Medic-Alert bracelet indicating her history Knowledge
deficit regarding management of bleeding , embolism & homecare

126. Facilitate learning processes; inform patient and significant others

of the following • Etiology • Effects • Common risk factors • Inform
patient and significant others about medications, side effects, dosage,
action etc. • Discuss and give patient list of signs and symptoms of excess
of anticoagulation

127. Health Education •Look for bleeding esp., with falls •Avoid use of
sharps •Use soft tooth brush •Don’t take aspirin and other O.T.C. drugs
while taking warfarin •Avoid use of laxatives •Report occurrence of dark
/tarry stool to health care provider immediately

128. Health Education •Describe strategies to prevent recurrent DVT/PE

•Avoid sitting with legs crossed or sitting for prolonged periods of time
•Follow the medication regimen •When traveling change position regularly,
walk occasionally, do active movement of legs and ankles while sitting
•Drink fluids esp. while traveling and in warm weather, to avoid
hemoconcentration due to fluid deficit

129. Health Education •Describe signs and symptoms of lower extremity

compromise; Homan’s sign, calf pain, edema, increased local temperature
etc. •Describe how and when to contact the health care provider if signs
and symptoms of circulatory compromise or pulmonary compromise are
identified.

130. Discharge and Home Care Guidelines Prevent recurrence. The nurse
should instruct the patient about preventing recurrence and reporting
signs and symptoms. Adherence. The nurse should monitor the patient’s
adherence to the prescribed management plan and enforces previous
instructions. Residual effects. The nurse should also monitor for
residual effects of the PE and recovery. Follow-up checkups. Remind the
patient about follow-up appointments for coagulation tests.

131. References •Harrison -18th edition •ACCP guidelines •Woods et

al:``Cardiac Nursing’’LIPPINCOTT •Brunner& Siddharth, Medical
Surgical Nursing’’ •Meg Gulanick et al:Nursing Care Plan 200,204

Definition: hernia is the protrusion of an organ, tissue or the part of an organ through the wall of the cavity that normally
contains it. Hernia

4. Weakness of the abdominal muscles. Increase intra abdominal pressure. Weakness of containing
membranes or muscles is usually congenital, or increases with age or due to any risk factors. Causes of hernia

5. Risk Factors Stretching of muscles during pregnancy. Obese people. Chronic constipation and straining during
a bowel movement or urination. Chronic hard coughing Improper heavy weight lifting.

6. Tight clothing and incorrect posture. Or because of scars from previous surgery. Many conditions increase
intra-abdominal pressure, (ascites, COPD, benign prostatic hypertrophy) Also, if muscles are weakened due to poor
nutrition, smoking, and overexertion.

7. 1-Hernia may be congenital or acquired: congenital hernias: occur prenatal or in the first year of life, and are caused
by a congenital defect. Acquired hernias: develop later on in life. 2- Hernia may be complete or incomplete: for example,
the stomach may partially or completely herniate into the chest. Classification of hernia

8. 3- Hernia may be internal or external: external ones herniate to the outside world, whereas internal hernias protrude
from their normal compartment to another.

9. 4. Hernia may be Reducible or Irreducible: • Reducible hernia: is one which can be pushed back into the abdomen by
putting manual pressure to it. • Irreducible hernia: is one which cannot be pushed back into the abdomen by applying
manual pressure.

10. Defect or weakness in the muscular wall may be congenital, acquired weakness or caused by trauma.
Increased the intraabdominal pressure as a result of any risk factors that discussed before. As a results of weakness
of the abdominal wall and increased pressure, the abdominal contents can protrude causing herniation
Pathophysiology of hernia:

11. When the contents of the hernial sac can be replaced into the abdominal cavity by manipulation, the hernia is said
to be reducible. Irreducible and incarcerated hernia refers to hernias that cannot be replaced by manipulation.
When the pressure from the hernial ring cuts off the blood supply to the herniated segment of the bowel, it becomes
strangulated.

12. Hernias can be classified according to their anatomical location into: • Abdominal hernias and diaphragmatic
hernias. (1) Inguinal hernia: • An inguinal hernia is a protrusion of abdominal cavity contents through the inguinal canal.
Types of hernia:

13. • -There are two types of inguinal hernia, direct and indirect. 1-Direct inguinal hernias: - This hernia passes through
the abdominal Wall in an area of muscular weakness not through a canal. - It occur medial to the inferior epigastric
vessels when abdominal contents herniate through a weak spot in the part of the posterior wall of the inguinal canal.

14. 2-Indirect inguinal hernias: occur when abdominal contents protrude through the deep inguinal ring, lateral to the
inferior epigastric vessels. • In female, the opening of the superficial inguinal ring is smaller than that of the male. As a
result, the possibility for hernias through the inguinal canal in males is common because they have a larger opening and
a much weaker wall for the intestines to protrude through it.

15. (2) Femoral hernia: • Femoral hernias occur just below the inguinal ligament, when abdominal contents pass into
the weak area at the posterior wall of the femoral canal. • They can be hard to distinguish from the inguinal type.
Femoral hernias are most common in women, especially those who are pregnant or obese.
16. (3) Umbilical hernia: • It is protrusion of intra abdominal contents through a weakness at the site of passage of the
umbilical cord through the abdominal wall. • These hernias often resolve spontaneously. • Umbilical hernias in adults
are acquired, and are more frequent in obese or pregnant women. There are three types of umbilical hernia:

17. 1- Para umbilical hernia: a type of umbilical hernia occurring in adults. It develop around the area of the umbilicus.
2- Congenital umbilical hernia 3- Acquired umbilical hernia

18. (4) Incisional hernia: • In an incisional hernia, the intestine pushes through the abdominal wall at the site of previous
abdominal surgery. • This type is most common in elderly or overweight people who are inactive after abdominal
surgery. •

19. (5) Hiatus hernia: Diaphragmatic hernia results when part of the stomach or intestine protrudes into the chest
cavity through a defect in the diaphragm. Hiatus hernias may be sliding or rolling

20. • Sliding hernia: in which the gastroesophageal junction and upper part of the stomach slides through the defect into
the chest. • Non-sliding : the junction remains fixed while another portion of the stomach moves up through the defect.
• Non-sliding hernias can be dangerous as they may allow the stomach to rotate and obstruct. • Repair is usually
advised.

21. • Patient with Sliding hernia have manifestations of reflux and complications of hemorrhage, obstruction and
strangulation can occur. • Patient with rolling hernia does not have manifestations of reflux as the gastrointestinal
sphincter is intact.

22. • Pathophysiology of haital hernia: • The diaphragm is a large dome-shaped muscle that separates the chest cavity
from the abdomen. • Normally, the esophagus passes into the stomach through an opening in the diaphragm called the
hiatus. • Hiatus hernias occur when the muscle tissue surrounding this opening becomes weak, and the upper part of
the stomach bulges up through the diaphragm into the chest cavity. • Also, pressure on the stomach may contribute to
the formation of hiatus hernia.

23. (6) Epigastric hernia: It is a protrusion of the epigastric contents through the abdominal wall. The protrusion occurs
between the linea Alba and the lower part of the rib cage in the midline of the abdomen.

24. 1) Bulging and painless swelling at first. 2) Pain: Pain may be: • Localized Pain: Pain may occur as a result of
irritation of or damage to area or nerves as a result of the hernia and its contents pushing into or pinching the nerves. •
Generalized Pain: If the contents of the hernia become trapped or incarcerated, the intestine's blood supply may
become compromised or shut off. Clinical manifestation of hernia:

25. • Referred Pain: • If the hernia irritates, inflames, the pain felt from the hernia may not be at the site of the hernia, but
rather at the area to which these nerves are traveling. • For example, pain from an Inguinal Hernia may be felt as
discomfort in the back, upper leg and /or hip area.

26. 3) Nausea and vomiting: • When intestine becomes trapped within the hernia, the normal flow of food through the
intestine becomes blocked. This creates a progressive back-up within the intestine and may result in nausea and
vomiting.

27. 4) Constipation: • If the intestine is blocked within the hernia, and normal flow of food contents and feces is blocked,
the patient may develop constipation. 5) Urinary Symptoms: • If the bladder becomes irritated within a hernia (usually
an Inguinal Hernia). Urinary symptoms such as frequency, urinary burning, frequent infections, and bladder stones may
all occur

28. Heartburn: occur 30 to 60 minutes after meals Difficulty in swallowing Fatigue Felling of fullness after
eating Difficulty of breathing Chest pain Clinical manifestation specific to hiatus hernia

29. 1) Medical treatment: • Hernias that are not strangulated can be mechanically reduced. • Truss (firm pad) held by a
belt to keep the hernia in place or reduced. • The patient is taught to apply the truss daily. • Instruct the patient to inspect
the skin under the truss for any manifestation of skin breakdown. Treatment

30. • If patient has preexisting medical conditions that make surgery unsafe, doctor may not repair hernia but will watch
it closely. • Some hernias have very large openings in the abdominal wall, and closing the opening is complicated
because of their large size. These kinds of hernias may be treated without surgery, using abdominal binders. • Some
doctors feel that the hernias with large openings have a low risk of strangulation. • An attempt to (push back) the hernia
will generally be made, often after giving medicine for pain and muscle relaxation

31. 2) Surgical treatment: 1) A hernia repair is performed using a small incision directly over the weakened area. The
intestine is then returned to the perineal cavity, the hernial sac excised and the muscle closed tightly over the area. 2)
Hernias in the inguinal region are usually repaired under spinal or local anesthesia.

32. 3) Some repair is difficult because there is insufficient muscle to keep the intestines in place. So steel mesh grafts
are used to reinforce the area of herniation 4) Clients with difficult repairs are usually hospitalized for 1 to 2 days to
receive prophylactic antibiotics. 5) If the intestinal contents of the hernia had the blood supply cut off, the development
of dead (gangrenous) bowel is possible in as little as six hours.
33. • The nurse encourages the patient to void immediately after surgery, because urinary retention is a common
problem. • Give prescribed medication as ordered. • The patient should be returned to general diet as soon as he
tolerates food. • Encourage post operative ambulation as soon as possible to prevent complications of immobility. •
Instruct the patient to avoid any risk factors that facilitate hernial recurrence. Post operative care

34. Management of haital hernia: • Provide small frequent diets that can pass easily through the esophagus. • Advise
the patient not to sleep for 1 hour after eating to prevent reflux.

35. • Paraesophageal hernia (Rolling haital hernia) may require emergency surgery to correct twisting of the stomach.
Postoperative Outcome: • Patients undergoing elective surgical repair may be able to go home the same day. However,
emergency repair carries a greater morbidity and mortality rate and this is directly proportional to the degree of bowel
compromise. Other co-existing medical conditions also influence outcome.

36. Complication of hernia: 1. Strangulation: pressure and compromise blood supply causing venous congestion
ischemia, and later necrosis and gangrene may occur. 2. Obstruction: for example, when a part of the bowel herniates,
bowel contents can no longer pass the obstruction. This results in cramps, vomiting, ileus, and absence of defecation.
3. Dysfunction: the herniated organ itself, or surrounding organs, start to malfunction

Classification • • • • Reducible Irreducible Obstructed/ Incarcerated Strangulated

9. Reducible Hernia • Characteristic signs – Reducibility – Cough impulse

10. Irreducible Hernia • Due to – Adhesions – Narrowing of neck – Incarceration – Massive hernia inside scrotum

11. Obstructed Hernia • Irreducibility + Intestinal obstruction • Features – No cough impulse – Irreducible – Painless –
Non tender – Features of intestinal obstruction

12. Strangulated Hernia • Blood supply of its contents impaired • Intestinal obstruction ± • Pathology – Intestinal
obstruction – Dilation of hernial contents – Impairment of venous return – Stasis --------- Arterial impairment

13. • Appearance – Congested and bright red – Ecchymosis – Extravasation of blood into lumen/ sac – loss of tone –
Translocation of gut bacteria – peritonitis/ sepsis – Gangrene

14. • Symptoms – Pain, vomiting – Ceases with onset of gangrene, ileus • Signs – Ill looking – Tense, tender –
Irreducible, no cough impulse – Acute intestinal obstruction – Peritonitis

15. Strangulated Omentocele • No features of intestinal obstruction • Gangrene onset delayed

16. Strangulated Richter’s Hernia • • • • Features mimic gastroenteritis Obstruction > 50 % of circumference Colic,
diarrhoes Constipation - ileus

17. Maydl’s Hernia • Retrograde strangulation • On opening sac – contents appear normal • Generalized peritonitis may
set in early

18. Inflamed Hernia • Outside – Abrasion, ill fitting truss • Inside – Diverticulitis, appendicitis • Signs of inflammation + •
Not associated with intestinal obstruction

19. INGUINAL HERNIA

20. Anatomy

21. Inguinal canal • • • • Triangular slit 3.75 cm long Above the inner half of inguinal ligament Deep to superficial inguinal
ring Developed due to the descent of testis in embryonic life

22. Deep Inguinal Ring • • • • Opening in the fascia transversalis 1.25 cm above mid inguinal point Medially – inferior
epigastric artery Spermatic cord in males; round ligament in females

23. Superficial Inguinal Ring • Aponeurosis of external oblique – crurae • Above and lateral to pubic crest • Spermatic
cord/ round ligament and illioinguinal nerves

24. • Anteriorly – skin, fascia, EO aponeurosis, lateral third – IO aponeurosis • Posteriorly – transversalis fascia, medial
½ conjoint tendon • Above – transversus abdominins and internal oblique fibres • Below – inguinal ligamnet

25. Contents • Illioinguinal nerves • Spermatic cord – Vas defrens – Testicular artery, art to vas defrens, cremasteric –
Pampiniform plexus of veins – Lymph vessels – Testicular plexus of sympathetic nerves, genital branch of
genitofemoral

26. Hassenbach’s Triangle • • • • • • Site of direct hernia Medially – lateral border rectus abdominis Laterally – inferior
epigastric vessel Inferiorly – inguinal ligament Floor – fascia transversalis Umbilical fold – obliterated umbilical artery
27. Mechanisms for preventing hernia • • • • • Obliquity of inguinal canal Shutter mechanism of fibres of IO, TA Sphincter
action of TA, IO at deep inguinal ring Ball valve action of cremasteric Fibres of internal oblique over deep inguinal ring
• Conjoint tendon

28. INDIRECT INGUINAL HERNIA • • • • More common Young individuals More common on the right side On basis of
extent – Bubonocele – Funicular hernia – Complete hernia

29. • Coverings – Peritoneum – Extraperitoneal fat – Internal spermatic fascia – Cremasteric fascia – External
spermatic fascia – Superficial fascia – skin

30. DIRECT INGUINAL HERNIA • • • • Directly through the hasselbach’s triangle Acquired (ex- Oglive hernia) More
common in elderly, malgaigne bulgings Rarely gets strangulated

31. • Symptoms – Pain/ discomfort – Lump – Systemic symptoms – obstruction, strangulation – Predisposing factors –
constipation, chronic bronchitis, urinary obstruction – Past history

32. • Signs – REDUCIBILITY – COUGH IMPULSE – Position – d/f femoral hernia – Get above the swelling –
Invagination test – Ring occlusion test

33. Rare Varieties • Interstitial hernia – Between muscle layers of abdominal wall – Commonly associated with
undescended testis – Preperitoneal – Intraperitoneal – Extraperitoneal

34. Rare Varieties • Sliding hernia – Older men – Extraperitoneal bowel with sac of peritoneum – Caecum, pelvic colon,
bladder – Strangulation of intestine within and outside the peritoneum • Richter’s • Maydl’s • Littre’s

35. TREATMENT • Conservative management • Surgical management

36. Conservative management : No Treatment • Indications – Severe ill health – Short life expectency – Refuse
operation

37. Conservative management : Truss • Indications – Refuse operation – Old patients with severe co morbidities –
Children ( c/I – undescended testis) • Contraindications – – – – – Irreducible hernia Undescended testis Chronic
bronchitits, strenous labour Associated with large hydrocele Not intelligent enough to position properly

38. • Dangers – Pressure atropht of muscles of inguinal region – Ostruction or strangulation – Used with partially
reduced hernia – may cause trauma – Improper cleanliness – unhealthy skin – Adhesions between sac and canal –
Chance of strangulation remains

39. Operative treatment • Herniotomy – Neck of sac transfixed, ligated and excised – Infants and children; young men
with good musculature • Herniorrhaphy – Herniotomy + repair of postrior wall – Indirect hernias – Adults with good
muscle tone

40. Hernioplasty • Herniotomy + reinforcement of posterior wall • Autologous – Fascia lata – External oblique
aponeurosis – Anterior rectus sheath flap – Skin flap – dermoplasty/ skin ribbon • Heterogenous – Prolene – Stainless
steel

41. • Indications – Indirect hernia – poor muscle tone – Direct hernia – Recurranthernia – Predisposing factors – chronic
cough,etc

42. Treatment of Strangulated Hernia • Emergency surgery • Resuscitation • Reduction of hernia – Foot end elevation –
Ice pack – NG, IV fluids – Analgesia, antibiotic

43. • Assess viability – Green/ black color – Flaccid , lustureless appearance – No peristalssis – Blood stained, foul
smelling fluid in sac • Bowel viable - HERNIORRHAPHY

44. • Bowel nonviable – Linear patch of gangrene – invagination – Loop of bowel – resection and anastomosis if gen
condition permits – Bowel large intestine – exteriorisation

45. RECURRENT INGUINAL HERNIA • Types of hernia – Sliding – Large/ long standing – Large direct hernia • Types
of patients – chronic cough • Inadequate preoperative preparation

46. RECURRENT INGUINAL HERNIA • Operative faults – – – – – Failure to ligate sac Tension in repair Use of
absorbable sutures Bleeding – infection Fault in selection of operation • Postoperative care – Wound infection – Lifting
heaavy weights – Persistence of predisposing factors • Appearance of new hernia

47. FEMORAL HERNIA

48. • Femoral ring – femoral canal – saphenous opening • More common in – Females – Old age • Most liable to
strangulate

49. Anatomy

50. Coverings of the sac of femoral hernia • • • • • • • Skin Superficial fascia Cribriform fascia Anterior layer of femoral
sheath Fatty contents of femoral canal Femoral septum Peritoneum
51. Rare types of femoral hernia • Prevascular hernia(Velpeu’s) – ass with posterior dislocation (Narath’s hernia) •
Retrovascular hernia Serafini • Pectineal hernia – Cloquet’s • External femoral hernia – Hesselbach’s • Lacunar hernia
– Lingier’s

52. • Symptoms – Swelling – Pain – Systemic symptoms • • • • Zeimenns technique Invagination technique Ring
occlusion test Position of swelling

53. Treatment • No conservative management • Surgery – herniorrhaphy – High operation(McEvedy’s) – Lottheissen’s

– Lockwood

54. UMBILICAL HERNIA • Three major types – Exomphalos – Umbilical hernia in infants and children – Paraumbilical
hernia in adults

55. Exomphalos • Minor – Small sac – Summit attached to the umbilical cord – Treatment • twisting of umbilical cord
and strapping

56. Exomphalos • Major • Umbilical cord attached to inferior aspect of swelling • Contains intestines, liver • Surgical
emergency • Immediate decompression and reduction

57. Umbilical hernia in children and infants • • • • Weak umbilical scar following neonatal sepsis Usually asymptomatic
90% cured within 12 – 18 months > 18 months – surgery

58. Paraumbilical hernia of adults • Supraumbilical or infraumbilical • Adhesions - seldom reducible • Predisposing
factors – – Women – Obesity – Repeated pregnancy • Treatment – Mayo’s operation

59. EPIGASTRIC HERNIA (Fatty Hernia of Linea Alba) • • • • Through fibres of linea alba Blood vessels pierce linea
alba Initially extraperitoneal fat only M.c. – young muscular men with strenous activity • Usually irreducible, no cough
impulse • If symptomatic - surgery

60. INCISIONAL HERNIA (Ventral Hernia) • Defect with patient – – – – Obesity Chronic cough perioperative period
Undue abdominal distention Malnutrition • Operative – – – – – Injury to nerves Careless wound closure Hemorrhage –
infection Tube drainage through laparotomy wound Midline infraumbilical

61. • Postoperative – Infection – Postop cough, distention – Postop peritonitis – Early removal of sutures – Postop
steroid therapy

62. Types of incisional hernia • Type 1 – Upper abdomen/ midline lower abdomen – Wide gap in musculature – Low risk
of strangulation • Type 2 – Lateral part of abdomen – Small defect – Strangulation risk high

63. Treatment • Prevention of incisional hernia – Weight reduction – Correct nutritional defects – Treat chronic cough –
Careful closure of abdomen – Prevent post op wound infection

64. • Conservative management – Reducible type 1 • SURGICAL MANAGEMENT

65. LUMBAR HERNIA • Superior lumbar hernia • Inferior lumbar hernia

66. Incisional lumbar hernia • Renal surgery with post op infection • Paralysis of lumbar muscles(phantom hernia) •
Treatment – Primary hernia – herniorrhaphy – Incisional hernia

67. OBTURATOR HERNIA • Rare; old women • Through obturator foramen • Thigh flexed, abducted and externally
rotated • Referred pain to knee joint • Strangulation - surgery

68. SPIGELEAN HERNIA • Interparietal hernia • At level of arcuate line, lateral to rectus • Treatment - surgery

69. • Gluteal hernia • Sciatic hernia

70. CONCLUSION • Protrusion of a part or whole of viscus through an abnormal opening in the wall of the cavity that
contains it • Inguinal hernia most frequent • Usual mode of treatment is surgical

Relaxation training Hypnotherapy Biofeedback training Cognitive/behavioral management Acupuncture

Nutritional supplements (B2 and others) Physical therapy and/or massage
cute Sinusitis

It is inflammation of sinuses , it is resolved promptly if their opening

into nasal cavity .

Clinical Manifestations

Pressure , pain over the sinus area

Tenderness

Purulent nasal secretions

29 Acute Sinusitis Medical Management Nursing management

Antimicrobial agent “Amoxicillin”

Oral & Topical Decongestant

Heated mist or Saline irrigation

Nursing management
“Teaching patient self care”

Complications

Meningitis &osteomylitis

Brain abscess

Ischemic infarction

30 Chronic Sinusitis

It is an inflammation of sinuses that persists for more than 8 weeks in

adult & or 2 weeks in children

Clinical Manifestations

Impaired mucociliary clearness & ventilation

Chronic hoarseness & cough

Chronic Headache

Facial pain

31 Chronic Sinusitis Medical Management Nursing Management

Strong antibiotics (for 21 days )

Surgical intervention to remove obstruction cause that cause block of

drainage passage

Nursing Management

Increase humidity

Increase fluid intake

Early signs of sinusitis

32 Acute Pharyngitis

It is a febrile inflammation of throat ,caused by virus about 70% ,

uncomplicated viral infection usually subsided promptly within 3-10 days

Clinical Manifestations

Fiery red pharyngeal membrane& tonsils

Lymphoid follicles that are swollen

Enlarge tender cervical lymph node

Fever & malaise

Sore throat , hoarseness,& cough

33 Acute Pharyngitis Medical Management

Supportive measures for viral infection

Pharmacologic therapy antibiotics for 10 days “cephalosporin”analgesic

for severe sore anti tussive medications

Nutritional therapy liquid or soft diet “If liquid can’t tolerated IV

fluid administered “

Nursing Management (bed rest ,skin assessment, mouth care &normal saline
gargle & self care teaching

34 Chronic Pharyngitis

Common in adults who work or live in dusty surrounding ,use the voice too
excess , suffer from chronic cough , & habitually use alcohol & tobacco

Types of pharyngitis

Hypertrophic :ch.ch.by general thickening& congestion of pharyngeal

mucus membrane

Atrophic : probably late stage of first type

Chronic Granular : ch.ch.by numerous swollen lymph follicles on the

pharyngeal wall

35 Chronic Pharyngitis Clinical Manifestations Medical Management

Constant sense of irritation or fullness in throat

Mucus expelled by coughing

Difficulty in swallowing

Medical Management

Relieving symptoms
Avoiding exposure to irritant

Correct respiratory & cardiac conditions

36 Chronic Pharyngitis Nursing Management 2. Antihistamine drugs

3. Decongestant

4. Controlling malaise

Nursing Management

Patient teaching of self care

Avoid alcohol , tobacco , exposure to cold

Face mask to avoid pollutant

Warm fluids,&warm saline gargle

37 Tonsillitis

The tonsils are composed of lymphatic tissue & situated on each side of
the oropharynx ,they frequently are the site of acute infection
(tonsillitis)

Clinical Manifestations

Tonsils : sore throat, fever , snoring & difficulty of swallowing

Adenoids : ear ache , mouth breathing , drainage ear ,frequent cold ,

bronchitis, noisy respiration, foul smelling breath &voice impairment

38 Tonsillitis Medical Management Nursing Management

For recurrent tonsillitis “tonsillectomy”

Conservative or symptomatic therapy

Antimicrobial therapy “penicillin” for 7 days

Nursing Management

Provide post op. care :V/S ,hemorrhage , position head turned to

side,water or ice chips

Teaching patient :S&S of hemorrhage

Avoid too much talking or coughing

Liquid or semi liquid diet for several days

Alkaline mouth washing with warm saline

39 Laryngitis Clinical Manifestations

It is an inflammation of larynx ,often occur as a result of voice abuse

or exposure to dust , chemicals , smoke , & other pollutants

Common in winter & easily transmitted

The cause of infection is almost virus

Clinical Manifestations

Hoarseness or aphonia

Severe cough

40 Laryngitis Medical Management Resting voice & avoid smoking

Inhale cool steam or an aerosol

Conservative treatment

Antibiotics for bacterial organisms

Nursing Management

Rest voice

Maintain a well humidified environment

Daily fluid intake

41 Pleurisy/Pleural Effusion

Pleurisy is a painful condition that arises from inflammation of the

pleura, or sac that encases the lung.

Pleural effusion occurs when the inflamed pleura secretes increased

amounts of pleural fluid into the pleural cavity.

42 Atelectasis
Collapse or airless condition of the alveoli caused
byhypoventilation,obstruction of airway or compression

Clinical Manifestations

Cough & sputum production

Dyspnea ,tachypnea ,tachycardia

Sings of pulmonary infection may present

Fever

Central cyanosis

43 Atelectasis Management

First line measures :(turning , early ambulation , lung volume expansion ,

coughing, spirometry ,breathing exercises

If there is no response : (PEEP , IPPB)

Bronchoscopy

Postural Drainage & percussion

If cause is compression remove the cause

44 Acute Tracheobronchitis

An inflammation of the mucus membrane of the trachea & the bronchial tree ,
often follow upper respiratory tract infection

Clinical Manifestations

Dry irritating cough “expectorate sputum”

Sternal soreness from coughing

Fever ,stress , night sweating

Headache & general malaise

As the infection progress the patient develop (shortness of breath, noisy

breath ,&purulent sputum

45 Acute Tracheobronchitis
Medical Management

Antibiotics depend on symptoms & culture

Expectorant may be prescribed

Increase fluid intake

Rest & cool therapy

Suctioning & Bronchoscopy

Nursing Management

Patient teaching

Encourage fluid intake

Coughing exercises to remove secretions

Complete antibiotics course,

Prevent over exertion

46 Pneumonia Community Acquired Pneumonia (CAP)

An inflammation of the lung tissue that is caused by microbial agent

Community Acquired Pneumonia (CAP)

Occurs either in community setting or within the first 48 hrs of

hospitalization

Most common in people younger than 60 yrs

Most prevalent during winter & spring

Caused by pneumococcus & H influenza

Virus the cause in infants & children

47 Pneumonia

Hospital Acquired Pneumonia (HAP) the onset of pneumonia symptoms more

than 48 hrs after admission to hospital. Also called nosocomial infection

Common organism E.colli ,Klebsiella ,S.aurious

It occurs when host defense impaired in certain conditions

Pneumonia in the Immuno compressed host

Caused by organisms also observed in CAP,HAP.

Has subtle onset with progressive dyspnea , fever , &productive cough

48 Pneumonia Clinical Manifestations Sudden onset of shaking chills

Rapidly increase in body temperature C

Chest pluratic pain increased by deep breathing

Patient looks severely ill with marked tachypnea

Shortness of breath

Orthopnea

Poor appetite

Diaphoresis &tires easily

Purulent sputum

49 Pneumonia Medical Management

Appropriate antibiotics depend on culture result

Hydration (increase fluid intake )

Antipyretic for fever & Headache

Warm moist inhalation to relieve irritation

Antihistamine to relieve sneezing & rhinorrhea

Oxygen & respiratory supportive measures

Complications : Shock & respiratory failure ,

Atelectasis & plural effusion

Super infection

50 Chronic Obstructive pulmonary Disease (COPD)

Disease state in which air flow is obstructed by emphysema or bronchitis

or both

The airway obstruction is usually progressive & irreversible

Clinical Manifestations

Cough

Increase work of breathing

Severe dyspnea that interfere with patient activity

51 Chronic Obstructive pulmonary Disease (COPD)

Medical Management

Inhaled bronchodilators to improve airway

Oxygen therapy as prescribed

Pulmonary rehabilitation emotional & physiologic needs ,breathing

exercises ,&methods of symptoms elevation

52 Chronic Obstructive pulmonary Disease (COPD)

Nursing Management

Patient Education About COPD

Breathing exercise

Inspiratory muscles training

Self care activity

Coping measures

Complications

Pneumonia

Atelectasis

Pneumothrax

Respiratory insufficiency & failure

53 Chronic Bronchitis

It is a productive cough that lasts in each of 2 consecutive years in a

patient whom other causes of cough is excluded

Clinical Manifestations
Chronic productive cough in winter

Increase frequency of respiratory infection

54 Chronic Bronchitis

Medical Management the objective of treatment are to keep the bronchioles

opened & functioning

Antibiotics therapy for recurrent infection

Bronchodilators to remove secretion

Postural Drainage & chest percussion

Hydration & fluid intake

Corticosteroid may be used

Smoker patient should stop smoking

55 Emphysema Classification

A complex and destructive lung disease wherein air accumulates in the

tissues of the lungs.

Smoking is the major cause of Emphysema

Classification

Panlobular : destruction of the respiratory bronchiole,alevular duct

&alveoli

Centrilobular : pathogenic changes take place mainly in the center of

secondary lobule

56 Emphysema Clinical Manifestations Increase dyspnea on exertion

Anoroxia & Weight loss

Weakness & Inactivity

Pursed –lip- breathing

Increase cough wheezing purulent sputum & occasionally fever

57 Emphysema Medical Management Bronchodilators Antimicrobial Agents

Oxygen therapy

Pulmonary rehabilitation

Smoking cessation

corticosteroids

58 Asthma

A condition characterized by intermittent airway obstruction in response

to a variety of stimuli. “inflammatory”

Asthma differ from COPD in that it is reversible process either

spontaneously or with treatment

Allergy is the strongest predisposing factor for the development of asthma

59 Asthma Clinical Manifestations

The most three common symptoms are: a- coug b- dyspnea c- wheezing

Hypoxemia may occur along with a- cyanosis b- diaphoresis c- tachycardia

d- widened pulse pressure

60 Asthma

Prevention : allergic test to identify the substances cause the symptoms

and avoid it as possible

Complications

Asthmaticus

Rib fracture

Pneumonia

Atelectases

61 Asthma Medical Management Peak flow monitoring

Pharmacologic Therapy (long term)

Corticosteroid :most effective ant inflammatory medication (inhaled
form)

Long-acting beta2adrenergic agonist mild to moderate bronchodilator

(theophilline

Quick relive medications (short acting beta2 adrenergic agonists

Peak flow monitoring

62 Asthma Nursing Management Immediate care based on severity of

symptoms

Assessment & Allergic History

Administer medication & observe patient response

Antibiotics as prescribed for infection

Assist in intubations procedure if needed

Psychological support for patient & his family

63 Acute Respiratory Failure

Conditions wherein there is a failure of the respiratory system as a whole.

It is a sudden & life threatening deterioration of gas exchange function

of the lung

Acute : a fall in arterial PaO2 to less than 50mmHg &a rise in arterial
PaCo2to greater than 50mmHg

64 Acute Respiratory Failure

Causes

Decrease respiratory derive “brain”

Dysfunction of chest wall “nerves & muscles”

Dysfunction of lung parenchyma “expansion”

Postoperative & inadequate ventilation

65 Acute Respiratory Failure

Clinical Manifestations

Impaired oxygenation & may be include restlessness

Fatigue & headache

Dyspnea & air hunger

Tachycardia &hypertension

Confusion & lethargy

Diaphoresis …… Respiratory Arrest

Uses of accessory muscles

66 Acute Respiratory Failure

Medical management:

Intubations and mechanical ventilation may be required to maintain

adequate ventilation and oxygenation while the case corrected

67 Acute Respiratory Failure

Nursing management:

Monitoring patient responses and arterial blood gases

Monitoring vital sign

turning ,mouth car , skin care , and rang of motion .

Teaching about the underlying disorders

Assists in intubations procedure

68 Pulmonary Embolism

Obstruction of a pulmonary artery by a bloodborne substance.

Deep vein thrombosis is a common cause of pulmonary embolism.

Other types (Air , Fat , Septic )

Clinical Manifestations

Dyspnea & Tachypnea

Sudden & pluretic chest pain

Fever & cough & hemoptesis

Apprehension Diaphoresis & syncope

69 Pulmonary Embolism Medical Management Emergency Management Nasal O2

IV infusion for Medication

Perfusion Scan

ABGs &ECG

Small dose of Morphine

Intubation & mechanical Ventilation

70 Pulmonary Embolism Pharmacologic Management

Anticoagulant therapy heparin bolus then 18u/kg/hrs warfarin for three

months

Thrombolytic therapy (STK , Actylase (TPA))

Surgical Management (Surgical Embolectomy)

71 Pulmonary Embolism Nursing Management Preventing thrombus formation

Monitoring thrombolytic therapy

Providing post operative nursing care

Managing O2 therapy

Preventing anxiety

Monitor for complications+

72 Pneumothorax/Hemothorax

Traumatic disorders of the respiratory tract wherein the underlying lung

tissue is compressed and eventually collapses.

Types

Simple Pnuemothrax
Traumatic Pnuemothorax

Tension

73 Pneumothorax/Hemothorax

Clinical Manifestations

Sudden pluretic pain

Anxious patient , dyspnea & air hunger

Increase use of accessory muscles

Central cyanosis

Tympanic sound in percussion

Absent of breath sound & tactile fremetus

Agitation Diaphoresis & hypotension

74 Pneumothorax/Hemothorax

Medical Management

High concentration supplemental O2

Chest tube for drainage

In emergency anything may be use to fill the chest wound

Heavy dressing

Needle aspiration thoracenthesis

Connecting chest tube to water seal drainage

An emergency thoractomy may also performed

75 Pulmonary Edema

A life-threatening condition characterized by a rapid shift of fluid from

plasma into the pulmonary interstitial tissue and the aveoli, resulting
in markedly impaired gas exchange.
Can result from severe left ventrical failure, rapid administration of
I.v. fluids, inhalation of noxious gases, or opiate or barbiturate
overdose.

76 Adult Respiratory Distress Syndrome

A life-threatening condition characterized by severe dyspnea, hypoxemia,

and diffuse pulmonary edema.

Usually follows major assault on multiple body systems or severe lung

trauma.

77 Bronchiectasis A chronic dilation of the bronchi.

Main causes of this disorder are pulmonary TB infection, chronic upper

respiratory tract infections, and complications of other respiratory
disorders of childhood, particularly cystic fibrosis.

78 Neoplasms of the Respiratory Tract

Benign neoplasms.

Lung cancer.

Cancer of the larynx.

79 Epistaxis A hemorrhage of the nares or nostrils.

May be unilateral (most common) or bilateral.

Blood loss can be minimal to severe.

80 Smoking

Cigarette smoking is indicated as a major causative factor in the

development of respiratory disorders, such as lung cancer, cancer of the
larynx, emphysema, and chronic bronchitis.

cute Sinusitis
It is inflammation of sinuses , it is resolved promptly if their opening
into nasal cavity .

Clinical Manifestations

Pressure , pain over the sinus area

Tenderness

Purulent nasal secretions

Medical Management

Antimicrobial agent “Amoxicillin”

Oral & Topical Decongestant

Heated mist or Saline irrigation

Tonsillitis

The tonsils are composed of lymphatic tissue & situated on each side of
the oropharynx ,they frequently are the site of acute infection
(tonsillitis)

Clinical Manifestations

Tonsils : sore throat, fever , snoring & difficulty of swallowing

Adenoids : ear ache , mouth breathing , drainage ear ,frequent cold ,

bronchitis, noisy respiration, foul smelling breath &voice impairment

26 Medical Management Nursing Management

For recurrent tonsillitis “tonsillectomy”

Conservative or symptomatic therapy

Antimicrobial therapy “penicillin” for 7 days

Nursing Management

Provide post op. care :V/S ,hemorrhage , position head turned to

side,water or ice chips

Teaching patient :S&S of hemorrhage

Avoid too much talking or coughing

Liquid or semi liquid diet for several days

Alkaline mouth washing with warm saline

Tonsillitis An inflammation (with infection) of the tonsils which can
cause significant edema of the tonsils occluding airway making the passage
of food (eating) and breathing difficult.

3 Tonsillitis

4 Etiology: caused by a bacteria or virus. Most common bacterial agent

is Group A beta hemolytic streptococcus. (GABHS).

5 Nursing Assessment: Causative agent diagnosed by throat culture. Strep

infection can be diagnosed in minutes using a “rapid strep” test.
Enlarged, reddened tonsils with or without exudates Sore throat,
difficulty swallowing due to sever sore throat Drooling caused by the
inability to swallow secretions Lymphadenopathy Mouth breathing With
strep child can have very distinct foul odor in their mouth (not always
but very frequent) Fever (can be quite high with strep)

6 Treatment: If viral, none supportive care only: promote comfort,

gargling with warm salt water, Tylenol/Motrin for pain, antiseptic throat
sprays, and throat lozenges. If Group A beta hemolytic strep: antibiotic
therapy. First choice of treatment is penicillin If PCN allergic:
erythromycin, azithromycin, clairthromycin In addition to antibiotic
therapy use supportive measures for comfort.

7 Nursing Interventions Patient teaching if bacterial infection stress

importance of finishing prescription, a complete course of prescribed
antibiotics is the only treatment for GABHS. Inadequate treatment of GABHS
can lead to rheumatic fever. Patients ( and parents have a tendency to
stop RX once the patient is feeling better)

8 Tonsillectomy Done when a child has a history of recurrent tonsillitis,

peritonsillar abscess or respiratory compromise from airway obstruction
(sleep apnea from very large tonsils). One of the most common surgical
procedures in the pediatric population. Can be done in ambulatory day
surgery unit or overnight (23) hour stay in hospital. Children must be
free of infection 1 week prior to surgery

9 Post operative Nursing care –AIRWAY, Airway, airway –Potential for

post operative edema, swelling – Monitor for s/s of bleeding frequent
or continual swallowing (child is trying swallowing blood from operative
site) Hemorrhage from surgical site, frank bleeding from nose, mouth,
between teeth.
10 Nuring interventions –Strict I &O NPO until awake & alert, then offer
clear fluid (H20), apple/white grape juice, yellow/green/orange Jell-O),
popsicles. Avoid all RED colored liquids & Jell-O, if child vomits it could
be mistaken for blood. Advance diet as tolerate to soft bland diet mashed
potatoes, macaroni & cheese, pudding, ice cream, oatmeal, farina etc…
When tolerating full po & has voided, IV is heplocked. –Pain Medication
Usually po/pr Tylenol with codeine.

11 Discharge Child can usually be discharged the next morning. These

procedures are frequently done as a 23 hour stay (admitted 9-10 am day
1, go to OR 12noon, return to floor 2pm, discharged 6-7am day 2 (to avoid
a Full day hospitalization, it is a way to get insurance companies to pay
for an overnight admission for observation but it is less than 1 full day
so it is cheaper)

Post operative Care Immediate general care Keep patient in coma

position until fully recovered from anaesthesia Keep watch on bleeding
from the nose and mouth Keep check the vital signs (HR,RR and BP) Diet
After fully recover ; cold milk or ice cream Sucking of ice cube gives
relief from pain Gradually from soft to solid food. Plenty of fluids
should be encourage

15. Oral Hygiene Pt. is given Condy’s or Salt water gargles 3-4 times
a day Mouth wash with plain water after every feed Analgesics Warn
patients that pain will abate during the first 3-5 days then increase for
1-2 days before completely disappearing Paracetamol can be taken to
relieve pain Antibiotics A suitable antibiotics can be given orally
or by injection for a week.

16. ComplicationsImmediate Delayed Primary heamorrhage Secondary

Reactionary haemorrhage haemorrhage Injury to tonsillar Infection
pillars, uvula, soft Lung complications palate, tounge or superior
Scarring in soft palate constrictor muscle and pillars Injury to teeth
Tonsillar remnants Aspiration of blood Hypertrophy of liangual
Facial oedema tonsil

Absolute Indications Recurrent infection of Tonsillitis causing

Febrile throat : seizures 7 > ep. In 1 year or Hypertrophy of tonsils
5 ep. / year for 2 years or causing : 3 ep. / year for 3 years or
Airway obstruction 2 weeks > of lost school or Difficulty in
deglutition work in 1 year Interference with speech Peritonsillar
abscess : Suspicion of malignancy In child - Done after 4-6 In
unilaterally enlarge weeks after abscess has tonsil suspect lymphoma been
treated in children and In adult - 2nd attack epidermoid carcinoma in
adults.

4. Relative Indications Diphtheria carriers, who do not respond with

antibiotics Streptococcal tonsillitis with bad taste or halitosis which
is unresponsive to medical treatment Recurrent streptococcal
tonsillitis in a patient with valvular heart disease.

5. The American Academy of Otolaryngology– Head and Neck Surgery

(AAO-HNS) Paraphrased, these clinical Relative indications
indicators are as follows: Three or more tonsil infections Absolute
indications per year despite adequate Enlarged tonsils that cause upper
medical therapy airway obstruction, severe Persistent foul taste or
breath due dysphagia, sleep disorders, or to chronic tonsillitis that is
not cardiopulmonary complications responsive to medical therapy
Peritonsillar abscess that is Chronic or recurrent tonsillitis in a
unresponsive to medical streptococcal carrier not management and drainage
responding to beta-lactamase- documented by surgeon, unless resistant
antibiotics surgery is performed during acute Unilateral tonsil
hypertrophy that stage is presumed to be neoplastic Tonsillitis
resulting in febrile convulsions Tonsils requiring biopsy to define
tissue pathology

6. Contraindication Anemia (Hb ↓ 10g%) Acute infections Bleeding

diathesis; leukaemia, purpura, aplastic aneamia, hemophilia Overt or
submucous cleft palate Children < 3 years of age Uncontrolled systemic
disease Tonsillectomy is avoided during the period of menses

hroat culture to determine the causative agent ,viral or bacterial as

GABHS.

Tonsillectomy & adenoidectomy (T&S) or (Ts &As).

Contraindicating for Ts &As: cleft palate, tonsillitis, blood disorder.

Nursing consideration:

Providing comfort & maintain minimize activities.

A soft or liquid diet is prescribed.

Warm salt water gargles

Analgesic, antipyretic.

23 Tonsillitis Post operative care:

Position (place child on abdomen or side).

Discourage child from coughing frequency.

Some secretion are common as dried blood.

Crushed ice& ice water to relief pain.

Analgesic may be rectally or IV, avoid oral route.

Avoid red or brown fluid, and citrus juice.

24 Tonsillitis Post operative care (cont.):

Soft food, milk or ice cream not offered.

Check post operative signs of Hemorrhage:

Increase pulse more than 120b/min.

Pallor.

Frequent swallowing.

Vomiting of bright blood

Decrease blood pressure is late sign of shock.

** Note: use good light to look direct on site of operation.

Post operative Nursing care –AIRWAY, Airway, airway –Potential for post operative edema, swelling – Monitor for s/s
of bleeding frequent or continual swallowing (child is trying swallowing blood from operative site) Hemorrhage from
surgical site, frank bleeding from nose, mouth, between teeth.

10 Nuring interventions –Strict I &O NPO until awake & alert, then offer clear fluid (H20), apple/white grape juice,
yellow/green/orange Jell-O), popsicles. Avoid all RED colored liquids & Jell-O, if child vomits it could be mistaken for
blood. Advance diet as tolerate to soft bland diet mashed potatoes, macaroni & cheese, pudding, ice cream, oatmeal,
farina etc… When tolerating full po & has voided, IV is heplocked. –Pain Medication Usually po/pr Tylenol with
codeine.

rsing Diagnosis for Tonsillitis

1. Acute pain related to the presence of inflammation in tosil.

2 · Imbalanced Nutrition Less Than Body Requirements related to
inadequate intake.

3 · Hyperthermia related to acute infection by microorganisms.

4 · Disturbed Sleep Pattern related to the pain in the tonsil area.

5. Anxiety related to a lack of knowledge or information about the illness

suffered by the client.

pproach Considerations
Treatment of acute tonsillitis is largely supportive and focuses
on maintaining adequate hydration and caloric intake and
controlling pain and fever. Inability to maintain adequate
oral caloric and fluid intake may require IV hydration,
antibiotics, and pain control. Home intravenous therapy
under the supervision of qualified home health providers or
the independent oral intake ability of patients ensures
hydration. Intravenous corticosteroids may be administered
to reduce pharyngeal edema.
Airway obstruction may require management by placing a
nasal airway device, using intravenous corticosteroids, and
administering humidified oxygen. Observe the patient in a
monitored setting until the airway obstruction is clearly
resolving
DNS It is very common. It requires treatment only if it produces
symptoms.

3. ETIOLOGY Heredity High arched palate Congenital Trauma Tumour,

mass or polyp in the nose

4. TYPES OF NASAL SEPTUM Normal Nasal septum C-shaped Nasal septum

S-shaped Nasal septum Displaced lower edge of septal cartilage

5. CLINICAL MANIFESTATIONS •Initially asymptomatic •Blocking of the nose

•Headache (Vacuum headache, neurologic headache) •Recurrent colds
•Anosmia •Epistaxis

6. DIAGNOSTIC TEST oAnterior rhinoscopy oPosterior rhinoscopy

7. COMPLICATIONS Recurrent sinusitis Middle ear infection Mouth

breathing Asthma Atrophic rhinitis

8. TREATMENT Submucous resection of the nasal septum (SMR) or Septoplasty

9. POST OP NURSING MANAGEMENT Antibiotic and analgesic administration for

5-8 days. Remove nasal packs after 48 hours. After removing nasal packs
use decongestants. Apply ointment, Vaseline or liquid paraffin in the nose
to loosen the crusts and clots. Advice to prevent injuries to the nose
for 3 weeks. And the patient must take one week rest. Forcible nasal
blowing must be avoided.
etiology 1. Trauma: blow on nose 2. Developmental: Birth moulding
High arched palate Unequal growth b/w skull base & palate 3. Mass in
opposite nasal cavity 4. Racial factors: common in Europeans 5. Hereditary:
in posterior D.N.S.

3. Types 1. Anterior / caudal dislocation 2. C-shaped deformity 3.

S-shaped deformity 4. Septal Spur: shelf-like projection 5. Septal
Thickening: organized hematoma or over-riding of septal fragments 6.
Impacted septum: despite decongestion

4. Clinical features 1. Nasal block: present on side of D.N.S. C/L

paradoxical nasal obstruction due to compensatory inferior turbinate
hypertrophy. 2. Recurrent cold: due to associated sinusitis 3. Headache:
due to contact with lateral wall (Sluder’s neuralgia), sinusitis

5. 13. Clinical features 4. Epistaxis: stretched mucosa on DNS dry

crusting & bleeding on removal; stretched blood vessels over spur. 5.
Hyposmia: seen in high D.N.S. 6. External nasal deformity

6. 14. Sequelae • Sinusitis • Mouth breathing snoring, pharyngitis •

Atrophic rhinitis & myiasis • Otitis media

ndications for septal surgery 1. D.N.S.: nasal obstruction / sinusitis

/ headache / epistaxis 2. Along with rhinoplasty 3. Harvesting of septal
cartilage graft 3. Trans-septal surgeries: Hypophysectomy Vidian
neurectomy 4. Hereditary telengiectasia

22. Septoplasty

23. Freer’s Incision

24. Cottle’s line Drawn from frontal spine to anterior nasal spine.
Deviations anterior to it can be treated by septoplasty only. Posterior
to it by SMR or septoplasty.

25. Muco-perichondrial flap elevation on right side

26. Anterior + Inferior tunnels

27. Inferior cartilage strip removal

28. Dislocation of bony cartilaginous junction

29. Muco-periosteal flap elevation on both sides

30. Cartilage + Bone removed

31. Scoring & cross-hatching

32. Wedge excision & shaving

33. Anterior nasal packing

34. Outer nasal packing

35. Submucosal Resection

36. Killian’s incision

37. Muco-perichondrial flap elevation on right side

38. Cutting of cartilage & elevation of opposite flap

39. Excision of septal cartilage

40. Excision of septal cartilage

41. Cartilage + Bone removed

42. Anterior nasal packing

43. S.M.R. Septoplasty Radical surgery Conservative Not done below 17 yr

Done after 4 yr Killian’s incision Freer’s incision Cannot correct
anterior DNS Can correct B/L mucoperichondrium elevated One side only
Radical removal of cartilage Only inferior strip Rhinoplasty incision
can’t combine Can Revision surgery difficult Relatively easy Cartilage
graft can be harvested No Complications common Rare

44. Complications of septal surgery 1. Haemorrhage 2. Septal haematoma

3. Septal abscess 4. Septal perforation 5. Saddle nose 6. Columellar
retraction 7. Flapping septum 8. Persistent deviation 9. Nasal synechia
10. C.S.F. rhinorrhoea 11. Infection 12. Toxic shock syndrome

45. Septal haematoma Collection of blood under perichondrium & periosteum

of nasal septum. Aetiology: 1. Nasal trauma 2. Septal surgery 3. Bleeding
disorders

46. Clinical features • Bilateral nasal obstruction • Sense of pressure

over nasal bridge • B/L smooth, rounded septal swelling • On palpation
mass is soft & fluctuant • Absence of raised temperature, erythema,
swelling & tenderness of skin over nose.

47. Septal Haematoma

48. Treatment 1. Small: wide bore needle aspiration 2. Large: a. incision

& drainage b. nasal packing (prevent recurrence) c. systemic antibiotics
(prevent abscess)
49. Complications • Thickened nasal septum • Septal abscess with cartilage
necrosis • Saddle nose • Supra-tip deformity • Septal perforation

50. Septal abscess Collection of pus under perichondrium & periosteum of

nasal septum. Aetiology: 1. secondary infection of septal hematoma 2.
following furuncle of nose or upper lip 3. following typhoid or measles

51. Clinical Features • Bilateral nasal obstruction with fever • Skin over
nose shows raised temperature, erythema, swelling & tenderness • B/L
smooth, soft, fluctuant septal swelling • Septal mucosa congested •
Submandibular node enlarged & tender

52. Septal Abscess

53. Septal abscess

54. Treatment • Abscess drained immediately • Incision made on most

dependent part • Pus & necrosed cartilage removed • Nasal packing done
• Systemic antibiotics for 10 days

55. Complications • Necrosis of septal cartilage • Saddle nose • Supra-tip

deformity • Septal perforation • Meningitis • Cavernous sinus thrombosis

56. Saddle nose

57. Nasal synechia

58. Perforated nasal septum

59. Aetiology 1. Trauma: septal surgery, nose picking, septal cautery,

ornamentation 2. Infection: septal abscess 3. Nasal Irritants: snuff,
cocaine 4. Foreign body, Rhinolith, Nasal myiasis 5. Granuloma: TB,
leprosy, syphilis, Wegener 6. Malignancy 7. Idiopathic

60. Clinical features Small perforation: whistling sound during

respiration Large perforation: nasal crusting nasal obstruction
epistaxis on crust removal

61. Perforated nasal septum

62. Treatment • Treat cause of septal perforation • Alkaline nasal douche

for crusting • Small perforation: closed by mucosal advancement flaps •
Large perforation: Silastic obturator, Alloderm. Results of surgery are

63. Nasal mucosal flaps

64. Nasal mucosal flaps

65. Sublabial flap

66. Silastic obturator

Pulmonary embolism (PE) refers to the obstruction of the pulmonary

artery or one of its branches by a thrombus (or thrombi) that originates
somewhere in the venous system or in the right side of the heart

3. Causes 1.thrombous 2. embolism 3.trauma 4. surgery 5.

hypercoaguability 6. heart failure 7. pregnancy ( increase
coaguability of BL 8. older than 50 years 9. atrial fibrillation

4. Pathophysiology -When a thrombus completely or partially obstructs

a pulmonary artery or its branches, the alveolar dead space is increased .
The area, although continuing to be ventilated, receives little or no
blood flow. Thus, gas exchange is impaired or absent in this area.

5. Pathophysiology -In addition, various substances are released from

the clot and surrounding area, causing regional blood vessels and
bronchioles to constrict. This causes an increase in pulmonary vascular
resistance. This reaction compounds (the ventilation–perfusion
imbalance.)

6. Pathophysiology -The hemodynamic consequences are increased

pulmonary vascular resistance from the regional vasoconstriction and
reduced size of the pulmonary vascular bed. This results in an increase
in pulmonary arterial pressure and, in turn, an increase in right
ventricular work to maintain pulmonary blood flow. When

7. Pathophysiology the work requirements of the right ventricle exceed

its capacity, right ventricular failure occurs, leading to a decrease
in cardiac output followed by a decrease in systemic blood pressure and
the development of shock.

8. RISK FACTORS Venous Stasis (slowing of blood flow in veins)

-Prolonged immobilization (especially postoperative) -Prolonged
periods of sitting/traveling -Varicose veins -Spinal cord injury
-Hypercoagulability (due to release of tissue thromboplastin after
injury/surgery) -Injury -Tumor (pancreatic, GI,, breast, lung)
-Increased platelet count (polysalathemia, splenectomy

9. RISK FACTORS Venous Endothelial Disease - -Thrombophlebitis

-Vascular disease -Foreign bodies (IV/central venous catheters)
-Certain Disease States (combination of stasis, coagulation alterations,
and venous injury) -Heart disease (especially heart failure) -Trauma
(especially fracture of hip, pelvis, vertebra, lower extremities)
10. RISK FACTORS -Postoperative state/postpartum period -Diabetes
mellitus -Chronic obstructive pulmonary disease c opD - Other
Predisposing Conditions -Advanced age -Obesity -Pregnancy -Oral
contraceptive use -Constrictive clothing -History of previous
thrombophlebitis, pulmonary embolism

11. Clinical Manifestations 1.Dyspnea is the most frequent symptom;

tachyapnea (very rapid respiratory rate) is the most frequent sign . The
duration and intensity of the dyspnea depend on the extent of embolization.
Chest pain is common and is usually sudden and pleuritic. It may be
substernal and misdiagnosed with angina pectoris or a myocardial
infarction. - Other symptoms include anxiety, fever, tachycardia,
apprehension, cough, diaphoresis, hemoptysis, and syncope.

12. Assessment and Diagnostic Findings -The diagnostic workup includes

a - ventilation–perfusion scan, -pulmonary angiography, -chest
x-ray -, ECG, -peripheral vascular studies, and arterial blood gas
analysis. -Doppler ultrasonography and venography

13. Prevention prevent deep venous thrombosis. 1. active leg

exercises 2. The intermittent pneumatic leg compression device ( reduces
venous stasis). 3. use of elastic compression stockings 4.
anticoagulant therapy

14. Medical Management • General measures to improve respiratory and

vascular status • Anticoagulation therapy • Thrombolytic therapy •
Surgical intervention

15. GENERAL MANAGEMENT -Oxygen therapy is administered to correct the

hypoxemia, relieve the pulmonary vascular vasoconstriction, and reduce
the pulmonary hypertension. -Using elastic compression stockings or
intermittent pneumatic leg compression devices reduces venous stasis.

16. GENERAL MANAGEMENT -These measures compress the superficial veins

and increase the vesecosity of blood in the deep veins by redirecting the
blood through the deep veins. Elevating the leg (above the level of the
heart) also increases venous flow.

17. Anticoagulation Therapy . Anticoagulant therapy (heparin, warfarin

sodium) has traditionally been the primary method for managing acute
deep vein thrombosis and PE

18. Anticoagulation Therapy Heparin is used to prevent recurrence of

emboli but has no effect on emboli that are already present. It is
administered as an intravenous bolus of 5,000 to 10,000 units, followed
by a continuous infusion initiated at a dose of 18 U/kg per hour, not to
exceed 1,600 U/hour

19. Thrombolytic Therapy -Thrombolytic therapy (urokinase, strepto-

kinase, alteplase, anistreplase, reteplase) also may be used in treating
PE, particularly in patients who are severely compromised (eg, those who
are hypotensive and have significant hypoxemia despite oxygen
supplementation). -

20. Thrombolytic Therapy Thrombolytic therapy resolves the thrombi or

emboli more quickly restores more normal hemodynamic functioning of the
pulmonary circulation, Reducing pulmonary hypertension Improving
perfusion, oxygenation, and cardiac output.

21. SURGICAL MANAGEMENT -Pulmonary embolectomy requires a thoracotomy

with cardiopulmonary by- pass technique. -Transvenous catheter
embolectomy is a technique in which a vacuum-cupped catheter is introduced
transvenously into the affected pulmonary artery. Suction is applied to
the end of the embolus and the embolus is aspirated into the cup .

22. Nursing Management MINIMIZINGTHE RISK OF PULMONARY EMBOLISM

PREVENTING THROMBUS FORMATION ASSESSING POTENTIAL FOR PULMONARY
EMBOLISM MONITORING THROMBOLYTIC THERAPY MANAGING PAIN

23. Nursing management MANAGING OXYGEN THERAPY RELIEVING ANXIETY

MONITORING FOR COMPLICATIONS PROVIDING POSTOPERATIVE NURSING CARE
PROMOTING HOME AND COMMUNITY-BASED CARE

24. Mention nursing process of patient have Pulmonary Embolism ?

DEFINE the following? thrombus Embolism Pulmonary vascular
resistance -Pulmonary arterial pressure-The intermittent pneumatic leg
compression device-Cardiopulmonary by pass technique