J G COLLEGE OF NURSING

AHMEDABAD
SUBJECT:ADVANCE
NURSING PRACTICE
TOPIC:case study

SUBMITTED TO
PROF.MR.YONATAN
LECTURER
J G COLLEGE OF NURSING
SUBMITTED BY
BINAL JOSHI
F Y MSC NURSING
J G COLLEGE OF NURSING
PATIENT’S BIODATA:

NAME : Mr. prakash shah

AGE : 33years

SEX : male

DOCTOR’S UNIT : Dr. Biren Hashvadan

DATE OF ADMISSION : 8 /11/2010

REGISTRATION NO : 68099

ADDRESS : 45,bandhan society

Sarkhej, Ahmedabad- 380082

MOBILE NO : 9567244120

MARITAL STATUS : Married

OCCUPATION : company worker

RELIGION : Hindu

NATIONALITY : Indian

DIAGNOSIS : congestive heart failure

HISTORY OF PATIENT:

CHIEF COMPLAINS:

Mr. vanaraj was admitted in medical intensive care unit of shalby hospital with the
complaints of vomiting since 2 days and abdominal pain since 1 day, history of altered
consciousness since today morning,, fever is also present. At the time of admission vital signs.
Respiration – gasping respiration. Pulse –
feasible pulse present. Temperature- 100F. Blood pressure- 80/ 40 mm of hg.
Emergency treatment given to the patient that is endotrachel intubation done and ventilator
support given by AMBU bag.
PRESENT HISTORY

Today patient is unconscious, not oriented to time, place and person, now also he is on
ventilator support .Central venous catheter is inserted using triple lumen catheter into internal
jugular vein ,iv fluids RL is going on. Chest leads applied on chest and attach with cardiac
monitoring. Cardiac monitoring is continuing. Today 1 episodes of vomiting in morning and
nausea also present. Blood pressure is decreased 80/40. So inj dopamine is going on via infusion
pump. Urinary catheter is present, urine output is 1800ml /day. His temperature sometimes get
high, it was 101 F, So antipyretic injection febrinil was given to him,

Vital signs

• Respiration :14breaths/min

• Pulse : 68beats/min

• Temperature :100 F

• Blood pressure: 100/50 mm of hg

• RBS : 410mg/dl

PAST HISTORY:

Mr.vanaraj has past history of diabetes mellitus since 10 years he is taking tab metformin
10 mg . no any other medical illness. He has no any surgical past history. Before 5 years he had
jaundice ,and before 3 years he had falisparum malaria also for that he had 2 times hospitalize
for treatment. He had complains had breathlessness along with chronic coughing, also he had
suffered from chronic constipation for that he was taking some ayurvedic tablets as per advised
by ayurvedic doctor.

PERSONAL HISTORY:

Mr.vanaraj ,he was admitted in Medical ICU on 8th November,2010 ;he is working in
company .His wife is housewife. He has two children one boy and one girl. He is belongs from
middle socioeconomic status. He is vegetarian. His has completed B.com. Total income of him is
15,000 /month. He is from Hindu religion so he is following all customs, rituals as pre Hindu. He
has habit of smoking and chewing tobacco. He looks young, well body built and always
enthusiastic to perform his tasks. Previousllly he did not look weak and lethargic than right now.
He is having good nature,responsibility towards his family members He says that I want
everybody should be happy as well as healthy in my family this information given by family
members.

FAMILY HISTORY:

His family is very social and has good relation with society member. Family also very
cooperative with all. He has two children one boy and one girl. He is belongs from middle
socioeconomic status. Her wife is having history of hyper tension since 1 year. No other family
members have no any major diseases like tuberculosis, ischemic heart diseases ,cancer ,asthma
allergy ,etc,

Family tree

Mr vanaraj Mrs. Maya

33 years 30 years

Mast. Mayank Ms. Hetal

9 year 6 year

MALE

FEMALE

SOCIOECONOMIC HISTORY:
 He is belongs from middle socioeconomic status. He was staying in village upto 22 years
then after marriage he was shifted to Ahmadabad. Total income family is 15,000 /month. He is
from Hindu religion so he is following all customs, rituals as pre Hindu. His family is very social
and has good relation with society member. Family also very cooperative. They have good
relationship with neighbor.

PHYSICAL ASSESSMENT

GORDEN’S DATA BASE ASSESSMENT:

Height :159cm

Weight:45 kg

Vital signs;

• Respiration :14breaths/min

• Pulse : 68beats/min

• Temperature :100 F

• Blood pressure: 100/50 mm of hg

• RBS : 410mg/dl

B) ORIENTATION TO UNIT:

Patient made to oriented as following:

• Call system : it is beside the patient.

• Side rails on bed :yes

• Meal /cafeteria hours : as patient is unconscious ryles tube feeding is given.

• Visitation Policy : Yes, explained to the relatives that the visiting hours is

from 12 noon to 1 pm and in evening time is 6 to 7 pm.

• Urination : Foleys catheter is inserted.

C) Health pattern Assessment:

1 .Reason for Hospitalization

Vomiting since 2 days and abdominal pain since 1 day, history of altered consciousness
since today morning, fever

2 .Recent illness or exposure to communicable disease

My patient had no previously any communicable disease.

3 .Previous Hospitalization or surgeries

Before 5 years he had jaundice, and before 3 years he had falisparum malaria also for that
he had 2 times hospitalize for treatment.

4 .What other problems you had?

He had complains had breathlessness along with chronic coughing, also he had suffered
from chronic constipation for that he was taking some ayurvedic tablets as per advised by
ayurvedic doctor.

5. Things done to manage health:

No necessary and adequate health steps were taken by individual in family to support him
or by patient himself.

6 .Statement of patient’s general appearance

Patient looks unconscious, not well oriented to time, place, person and environment, not
following verbal commands.

7. Tobacco use:

He did not take tobacco in any kind of extra form except 10-15 bidis per day.

8. Allergies:

No any allergy to any drug or no sensitivity to any other drugs.

9. Food:

He likes to eat green leafy vegetables, fruits, chapatti and milk, pulses, salad etc; He has no
any food allergy.

10. MEDICATION:

• Inj Human insulin 15 units SC before lunch and before dinner

 • Inj cefotaxim 2 g every 4 hrly.

• Inj voveran 25 mg IV bd

• Inj Pantodac 40 mg IV bd

• Inj dopamine 200mg+NS 40 cc IV 4 ml /hour running in infusion pump.

• Inj Noradrenaline 2mg+NS 48 cc IV running in infusion pump

• Inj Emset 4 mg IV 8 hrly

• Inj DNS 40 ml IV running in pint.

11. Have you been taking your medications as been prescribed?

Yes

12. Other patient data: not applicable

2. NUTRITION / METABOLIC ASSESSMENT:

Patient is on ventilator so he is on nil per mouth status.

• SUPPLEMENTS:
No any supplements to be taken by the client

• PATTERN OF DAILY FOOD/FLUID INTAKE

He is on nil per mouth. So IV fluid is going on like DNS and RL.
• APPETITE: normal
• WEIGHT LOSS/GAIN: loss 1.2 kg
• NAUSEA/VOMITING: yes
• GI PAIN: no
• CONDITION OF THE ORAL MUCUS MEMBRANE : good no ulcers or
nfection
• DENTAL CONDITION: all teeth is present
• DENTURES: present
• SKIN :warm and dry
• TURGOR: fragile
• COLOR: pale
• EDEMA : no
• WOUND/DRAIN /DRESSINGS: no
 • SKIN PROBLEMS: no
• I V’S: yes
• OTHER PATIENT DATA: --

3. ELIMINATION:

• ABDOMINAL TENDERNESS: present

• BOWEL SOUNDS: Not applicable

• STOMA: Not applicable

• ANY PROBLEM WITH HEMORROIDS/INVOLUNTARY STOOL: Not applicable

• USUAL BOWEL PATTERN

Client usually goes in the morning for the defecation usually once a day.

• DATE OF LAST BM :12-11- 10

• IF PROBLEM DESCRIBE :no problem

• USE OF ANY THING TO MANAGE BOWELS: not applicable

• USUAL URINARY PATTERN

Client is usually suffering from diabetes .so she is having excessive thirst and same way
urination. So he goes frequently for the urination

• LAST VOID: in the morning

• IF PROBLEM DESCRIBE: no problem

• PERSPIRATION/NOCTURAL SWEATS: Not applicable

• OTHER PATIENT DATA: Not applicable

4. ACTIVITY /EXERCISE

CARDIOVASCULAR STATUS

• PERIPHERAL PULSES: 82beats/min

• NEUROVASCULAR CHECK: capillary refill 2 sec

• CHEST PAIN/RADIATION: no
 • JUGULAR VEIN DISTENTION: no

• HX OF MURMUR: no

• PACEMAKER: no

• PRESENCE OF AV SHUNT: no

• ATRIOVENOUS BRUIT : no

• HEMODYNAMIC MONITORING:

SPO2- 96%

BLOOD PRESSURE- 110/30 mm of hg

RESPIRATION – 15breaths of ventilator

TEMPERATURE- 100 F

PULSE- 82 beats/min

ECG- normal
-Normal sinus rhythm of heart rate ,no tachycardia,no tachypna,bradycardia or no
bradypnea

-Left ventricular ejection fraction is 60%

-No evidence of chest pain .

• PERIPHERALSMEAR EXAMINATION: wbc shows polymorphoneclear

leucocytosis

RESPIRATORY STATUS

• RESPIRATORY PATTERN: gasping respiration after kept on ventilator

normal breathing pattern

• S.O.B ON EXERTION: present

• OTHER: Not applicable

• LUNG SOUNDS: On auscultation normal lung sounds were present. Along with
few crepitation sounds in rright and left lower zone of
Lungs. No evidence of rhonchi or wheezing sound.

• USE OF ACCESSORY MUSCLES:present

• COUGH/PRODUCTION : on ventilator patient having excessive secretions that
are sticky and thick in consistency ,white in colour,so daily every 4 hrly
 suctioning is done regularly ,taking care Of him without harming to mucous
membranes and to facilitate cough secretions nebulization is given along with
duolin and budecort alternately

• RESPIRATORY TUBES: endotracheal tube inserted and attach with ventilator

• VENTILATORY ASSISTANCE: yes

5. COGNITIVWE OR PERCEPTUAL ASSESSMENT:

• LEVEL OF CONSCIOUOSNESS: on admission he was unconscious

and disoriented ,so he was intubaed on 8th November at 11o’clock

• BEHAVIOUR: He is unconscious. So I cannot able to assess the

behaviour.

• HISTORY OF EPILEPSY AND SEIZURES:Not present and no history

of parkinson’s disease

• REFLEXES:

o Eye: Pupil size Normal in both eyes

o Pupillary reaction: equal in both eyes

o Accomodation: within normal limits

No deviation found either in right or in left eye

Not having cataract or previous eye operation

No myopia or hypermetropia

HANDGRASP : present

GAG REFLEX : present

SWALLOWING REFLEX :present

• MOVEMENT OF EXTREMITIES: PRESENT

• SENSORIUM FUNCTION:

• Eyes/sight : no cataract in both yes but hypermetropia is

present
 • Ears/hearing : He is unconscious. So I cannot able to assess

• Nose/smell :He is unconscious. So I cannot able to assess

• Tongue/taste : He is unconscious. So I cannot able to assess

Numbness/tingling :no problem

• Dizziness not present

• PAIN

He has abdominal pain before 2 days.

• COGNITION ASSESSMENT

• Primary language: gujarati

• Speech deficit: No problem

• Aid : not using

• Any learning difficulties: Now not able to learn new things

6. SLEEP OR REST ASSESSMENT:

At home adequate amount of sleep,but disturbed sometimes only because frequent

urination at night.

7. SELF CONCEPT OR PERCEPTION:

• ARE THERE ANY WAYS YOU FEEL DIFFERENTLY ABOUT YOUR

SELF SINCE YOU HAVE BEEN HOSPITALIZED OR ILL:

Patient is unconscious

• DESCRIPTION OF NONVERBAL BEHAVIOUR: Patient is unconscious

• OTHER PATIENT DATA:--

8. ROLE/RELATIONSHIP

• MARRITAL STATUS; MARRIED

• CHILDREN: two boys

• DO YOU LIVE ALONE/WITH FAMILY/OTHER: with family

• FAMILY FEELINGS REGARDING HOSPITALIZATION:her both the child is

very attached to him and cares for him .they are worried about their father and
participates in him care. They want that their father will be again healthy and
independent.

• WHO ARE THE PEOPLE THAT WILL HELP YOU MOST AT THIS TIME:
his wife

• ARE YOU PRESENTLY EMPLOYED: yes, get the information from his wife

• ARE YOU PRESENTLY IN SCHOOL: no

• OTHER PATIENT DATA:

9. COPING OR STRESS:

• HAVE EXPERIENCED ANY RECENT SITUATION IN ADDITION TO

YOUR ILLNESS : not applicable

• IF YES PLEASE DESCRIBE: not applicable

• ARE THERE ANY WAYS WE CAN BE OF ASSISTANCE : not applicable

• HOW DO YOU USUALLY MANAGE THE STRESS: not applicable

• WHAT DO YOU DO FOR RELAXATION: not applicable

• SUPPORT GROUPS /COUNCELLLING RESOURCES USED: not applicable

10. VALUE/BELIEF

WILL ILLNESS/HOSPITALIZATION INTERFERE WITH ANY OF THE

FOLLOWING?

• SPIRITUAL OR RELIGIOUS PRACTICES: not applicable

• CULTURAL BELIEFS OR PRACTICES: not applicable

 • FAMILY TRADITIONS: not applicable

• WOULD YOU LIKE TO CONTACT HOSPITAL AUTHORITY : not applicable

• OTHER PATIENT DATA:--

11. IMPRRESSION:

-Possible nursing diagnostic concepts to consider for care planning;

• impaired gas exchange related to excessive mucus secretion as evidenced by frequent

suctioning and low saturation of oxygen.

• Alteration in thermoregulation, fever related to presence of infection and due to low

immunity as evidenced by checking temperature.

• Activity intolerance related to immobility as evidenced by stiffness of the joints.

• Imbalanced nutrition less than body requirement related to vomiting and nausea as
evidenced by checking skin turgor.

• Risk for infection related to invasive procedure like insertion of ET tube as evidence by
increased WBC count.
ANATOMY AND PHYSIOLOGY:

• Anatomy and function of the Pancreas

 Pancreas glandular organ that secretes digestive enzymes and hormones. In

humans, the pancreas is a yellowish organ about 7 in. (17.8 cm) long and 1.5 in.
(3.8 cm) wide.
 It lies beneath the stomach and is connected to the small intestine at the
duodenum.
 Most of the pancreatic tissue consists of grapelike clusters of cells that produce a
clear fluid (pancreatic juice) that flows into the duodenum through a common
duct along with bile from the liver. Pancreatic juice contains three digestive
 enzymes: tryptase, amylase, and lipase, that, along with intestinal enzymes,
complete the digestion of proteins, carbohydrates, and fats, respectively.
Scattered among the enzyme-producing cells of the pancreas are small groups of
endocrine cells, called the islets of Langerhans, that secrete two hormones,
insulin and glucagon.
 The pancreatic islets contain several types of cells: alpha-2 cells, which produce
the hormone glucagon; beta cells, which manufacture the hormone insulin; and
alpha-1 cells, which produce the regulatory agent somatostatin.
 These hormones are secreted directly into the bloodstream, and together, they
regulate the level of glucose in the blood. Insulin lowers the blood sugar level and
increases the amount of glycogen (stored carbohydrate) in the liver; glucagon has
the opposite action.
 Failure of the insulin-secreting cells to function properly results in diabetes,
which can occur in two major forms, the division being between juvenile onset
and onset in maturity. Pancreatic cancer has a particularly high mortality rate, and
patients with a family history of the disease sometimes have the pancreas
removed if precancerous cysts are present in the organ.
 Every cell in the human body needs energy in order to function. The body’s
primary energy source is glucose, a simple sugar resulting from the digestion of
foods containing carbohydrates (sugars and starches).
 Glucose from the digested food circulates in the blood as a ready energy source
for any cells that need it. Insulin is a hormone or chemical produced by cells in
the pancreas, an organ located behind the stomach.
 Insulin bonds to a receptor site on the outside of cell and acts like a key to open a
doorway into the cell through which glucose can enter. Some of the glucose can
be converted to concentrated energy sources like glycogen or fatty acids and
saved for later use.
 When there is not enough insulin produced or when the doorway no longer
recognizes the insulin key, glucose stays in the blood rather entering the cells.
INSULIN EFFECTS: HOW DOES INSULIN LOWER BLOOD SUGAR LEVELS

 Although insulin plays a vital role in the regulation of carbohydrate, fat and protein
metabolism, it is probably best known for its ability to lower blood sugar levels. So how
exactly does insulin reduce blood glucose levels?
 Immediately after a meal, sugar in the blood stream stimulates the secretion of insulin
from the pancreas which then goes about clearing the sugar from the blood stream by
promoting its absorption, utilization and storage by tissues of the body. Insulin effects
mainly include:

• Promoting glucose uptake and use by muscles

• Promoting glucose uptake, use and storage by liver cells

Insulin Effects on Muscles to Reduce Blood Glucose Levels

 The first thing to understand is that glucose is a substance used by cells to produce energy
required for activities of the body. Muscle cells do not usually utilize blood glucose, even
when its concentration is high in circulation, preferring instead to use fatty acids to
produce energy required by them.
 But under the influence of insulin, muscle cells rapidly absorb glucose and use it to fuel
their actions. This happens immediately after a meal when insulin secretion is high. The
only other time muscle cells use up glucose in the blood stream, even in the absence of
insulin, is during exercise.
  But what happens when the body is resting after a meal and insulin is actively
transporting sugar into muscle cells? These glucose molecules are strung together to form
glycogen, the storage form of glucose. Glycogen is stored in muscle tissue for later use,
especially when muscles require lots of energy for short spurts of strenuous activity.
 In a similar manner, insulin helps glucose uptake and use by most other cells in the body,
except the brain cells.

Insulin Effects on Liver to Lower Blood Sugar

 One of the important functions of the liver is to act as a storehouse for energy. Under the
influence of insulin, most of the glucose absorbed from a meal is transported into the liver
where it is converted into and stored as glycogen.
 When the body requires energy in between meals, glycogen from the liver stores is
broken down and glucose released into circulation. High blood glucose levels cause
insulin secretion which promotes glucose storage in the liver, whereas low blood sugar
levels inhibit insulin secretion, causing glucose stores to be broken down and returned to
the blood.

Blood Glucose Regulation – Conversion of Glucose into Fatty Acids

 Unfortunately, there is a limit to the capacity of the liver to store glycogen. So what
happens when this limit is exceeded? Insulin causes the excess glucose to be converted
into fatty acids which are then released into circulation as very low density lipooroteins
(VLDL). These find their way to fat stores in the body called adipose tissue. This goes a
long way in explaining how high carbohydrate diets cause fat deposition in the body.
 Insulin also promotes fat deposition by uptake of glucose by adipose (fat) cells where it is
used to form the glycerol part of the fat molecule.

Insulin Effects on Brain Cells

 Interestingly, brain cells do not depend on insulin at all. They only use glucose for energy
production (unlike other cells which can also use fatty acids and other substrates) which
they directly absorb from the blood, independent of insulin. When the glucose level falls
below a critical level, brain cells suffer by going into hypoglycemic shock.
 In diabetes mellitus, where there is either a lack of insulin or resistance to its action,
glucose metabolism is severely impaired. Most of the cells are unable to use glucose,
except, fortunately, the brain cells.
 Insulin effects on muscle, liver and adipose tissue help lower blood sugar levels by
glucose uptake, use and storage. Insulin therefore plays a vital role in blood glucose
regulation and maintaining normal blood glucose levels.
 DIABETIC KETOACIDOSIS

INTRODUCTION

Diabetic ketoacidosis (DKA) is a state of absolute or relative insulin deficiency aggravated by

ensuing hyperglycemia, dehydration, and acidosis-producing derangements in intermediary
metabolism. The most common causes are underlying infection, disruption of insulin treatment,
and new onset of diabetes.Diabetic ketoacidosis is typically characterized by hyperglycemia over
300 mg/dL, low bicarbonate level (<15 mEq/L), and acidosis (pH <7.30) with ketonemia and
ketonuria. While definitions vary, moderate DKA can be categorized by pH <7.2 and serum
bicarbonate <10 mEq/L, whereas severe DKA has pH <7.1 and bicarbonate <5 mEq/L. Mental
status changes can be seen with mild-to-moderate DKA with more severe deterioration in mental
status typical with moderate-to-severe DKA.

DEFINATION

Diabetic ketoacidosis is a complication of diabetes that occurs when the body cannot use
sugar (glucose) as a fuel source because the body has no insulin or not enough insulin, and fat is
used instead. Byproducts of fat breakdown, called ketones, build up in the body.

Diabetic ketoacidosis is a metabolic derangement in TYPE 1 diabetis that results from a

deficiency of insulin . highly acidic ketone bodies are formed , resulting in acidosis, usally
requires hospitalisation for treatment and is usally caused by nonadherence to the insulin regiman
, concurrent illness, or infection.

INCIDENCE

AS PER TEXT BOOK AS PER PATIENT

• How ever , mortality rates have My patient is 33 years old.

declined during this same period. It
occur most frequently in teenagers and
older adults.
• Diabetic ketoacidosis occurs primarily
in patients with type 1 diabetes. The
incidence is roughly 2 episodes per 100
patient years of diabetes, with about
3% of patients with type 1 diabetes
initially presenting with diabetic
ketoacidosis. It can occur in patients
with type 2 diabetes as well; however,
this is less common.

• People with type 2 diabetes can

develop ketoacidosis, but it is rare. It is
 usually triggered by a severe illness.
People of Hispanic and African-
American ethnicity seem to be more
likely to have ketoacidosis as a
complication of type 2 diabetes.

ETIOLOGY

AS PER TEXT BOOK AS PER PATIENT

• The most common scenarios for

diabetic ketoacidosis are underlying or
concomitant infection (40%)
• missed insulin treatments (25%), and
newly diagnosed
• previously unknown diabetes (15%).
Other associated causes make up
roughly 20% in the various series.
• Urinary tract infections (UTIs) are the
single most common infection
associated with diabetic ketoacidosis
• But many other associated illnesses
need to be considered as well.

 Myocardial infarction
 Cerebrovascular accident
 Complicated pregnancy
 Trauma
 Stress
 Cocaine
 Surgery
 Heavy use of concentrated
carbohydrate beverages such as
sodas and sports drinks
 Acromegaly
 Idiopathic (20-30%)
 Dental abscess1

• As fats are broken down, acids called

ketones build up in the blood and urine.
In high levels, ketones are poisonous.
This condition is known as
ketoacidosis
 • Blood glucose levels rise (usually
higher than 300 mg/dL) because the
liver produces glucose to try to combat
the problem. However the cells cannot
pull in that glucose without insulin.

PATHOPHYSIOLOGY:
• Many of the underlying pathophysiologic disturbances in diabetic ketoacidosis (DKA) are
directly measurable by the clinician and need to be monitored throughout the course of
treatment. Close attention to clinical laboratory data allows for tracking of the underlying
acidosis and hyperglycemia as well as prevention of common potentially lethal
complications such as hypoglycemia, hyponatremia, and hypokalemia.

• The absence of insulin, the primary anabolic hormone, means that tissues such as muscle,
fat, and liver do not take up glucose. Counterregulatory hormones, such as glucagon,
growth hormone, and catecholamines, enhance triglyceride breakdown into free fatty
acids and gluconeogenesis, which is the main cause for the elevation in serum glucose
level in diabetic ketoacidosis. Beta-oxidation of these free fatty acids leads to increased
formation of ketone bodies. Overall, metabolism in diabetic ketoacidosis shifts from the
 normal fed state characterized by carbohydrate metabolism to a fasting state characterized
by fat metabolism.

• Secondary consequences of the primary metabolic derangements in diabetic ketoacidosis

include an ensuing metabolic acidosis as the ketone bodies produced by beta-oxidation of
free fatty acids deplete extracellular and cellular acid buffers. The hyperglycemia-induced
osmotic diuresis depletes sodium, potassium, phosphates, and water as well as ketones
and glucose.
• Patients are often profoundly dehydrated and have a significantly depleted potassium
level (as high as 5 mEq per kg of body weight). A normal or even elevated serum
potassium concentration may be seen due to the extracellular shift of potassium in
acidotic conditions, and this very poorly reflects the patient's total potassium stores. The
serum potassium concentration can drop precipitously once insulin treatment is started, so
great care must be taken to repeatedly monitor serum levels. Urinary loss of ketoanions
with brisk diuresis and intact renal function may also lead to a component of
hyperchloremic metabolic acidosis.

CLINICAL MANIFESTATION

AS PER TEXT BOOK AS PER PATIENT

• Classic symptoms of hyperglycemia

o Thirst
o Polyuria, polydipsia
o Nocturia
• Other symptoms
o Generalized weakness
 o Malaise/lethargy
o Nausea/vomiting
o Decreased perspiration
o Fatigue
o Anorexia or increased appetite
o Confusion
• Symptoms of associated infections and
conditions
o Fever
o Dysuria
o Chills
o Chest pain
o Abdominal pain
o Shortness of breath

• General signs
o Ill appearance
o Dry skin
o Labored respirations
o Dry mucous membranes
o Decreased skin turgor
o Decreased reflexes
• Vital signs
o Tachycardia
o Hypotension
o Tachypnea
o Hypothermia
o Fever, if infection
• Specific signs
o Ketotic breath (fruity, with
acetone smell)
o Confusion
o Coma
o Abdominal tenderness

DIAGNOSTIC TEST

AS PER TEXT BOOK AS PER PATIENT

 History collection
 Physical examination
 Ketone testing may be used in type 1
 diabetes to screen for early
ketoacidosis. The ketones test is done
using a urine sample. Ketone testing is
usually done at the following times:

• When the blood sugar is higher

than 240 mg/dL
• During an illness such as
pneumonia, heart attack, or stroke
• When nausea or vomiting occur
• During pregnancy
• Ketonuria

• Other tests that may be done to

diagnose ketoacidosis include:

• Arterial blood gas

• Blood glucose test
• Blood pressure measurement
• Amylase blood test
• Potassium blood test

• This disease may also affect the results

of the following tests:

• CO2
• CSF collection
• Potassium urine test
• Magnesium blood test
• Phosphorus blood test
• Sodium blood test
• Sodium urine test
• Urine pH

MEDICAL MANAGEMENT

AS PER TEXT BOOK AS PER PATIENT

The main aims in the treatment of diabetic

ketoacidosis are

 replacing the lost fluids and

electrolytes while suppressing
 the high blood sugars and
ketone
 production with insulin.
 Admission to an intensive care
unit or similar high-dependency
area or ward for close
observation may be necessary.

Fluid replacement

• The amount of fluid depends on the

estimated degree of dehydration. If
dehydration is so severe as to cause
shock (severely decreased blood
pressure with insufficient blood supply
to the body's organs), or a depressed
level of consciousness, rapid infusion
of saline (1 liter for adults, 10 ml/kg in
repeated doses for children) is
recommended to restore circulating
volume. Slower rehydration based on
calculated water and sodium shortage
may be possible if the dehydration is
moderate, and again saline is the
recommended fluid. Very mild
ketoacidosis with no associated
vomiting and mild dehydration may be
treated with oral rehydration and
subcutaneous rather than intravenous
insulin under observation for signs of
deterioration.
• A special but unusual consideration is
cardiogenic shock, where the blood
pressure is decreased not due to
dehydration but due to inability of the
heart to pump blood through the blood
vessels. This situation requires ICU
admission, monitoring of the central
venous pressure (which requires the
insertion of a central venous catheter in
a large upper body vein), and the
administration of medication that
increases the heart pumping action and
blood pressure.[1]
Insulin

• Some guidelines recommend a bolus

(initial large dose) of insulin of 0.1 unit
of insulin per kilogram of body weight.
This can be administered immediately
after the potassium level is known to
be higher than 3.3 mmol/l; if the level
is any lower, administering insulin
could lead to a dangerously low
potassium level (see below). Other
guidelines recommend delaying the
initiation of insulin until fluids have
been administrered.
• In general, insulin is given at
0.1 unit/kg per hour to reduce the
blood sugars and suppress ketone
production. Guidelines differ as to
which dose to use when blood sugar
levels start falling; some recommend
reducing the dose of insulin once
glucose falls below 16.6 mmol/l
(300 mg/dl)[1] but other recommend
infusing glucose in addition to saline to
allow for ongoing infusion of higher
doses of insulin.[9][5]

Potassium

• Potassium levels can fluctuate severely

during the treatment of DKA, because
insulin decreases potassium levels in
the blood by redistributing it into cells.
Serum potassium levels are initially
often mildly raised even though total
body potassium is depleted—as
potassium from the intracellular space
would have been shifted to the
extracellular space in an exchange for
hydrogen ions that accumulate
extracellularly in acidosis of DKA. A
large part of the shifted extracellular
potassium would have been lost in
 urine because of osmotic diuresis.
Hypokalemia (low blood potassium
concentration) often follows treatment.
This increases the risk of dangerous
irregularities in the heart rate.
Therefore, continuous observation of
the heart rate is recommended,[9] as
well as repeated measurement of the
potassium levels and addition of
potassium to the intravenous fluids
once levels fall below 5.3 mmol/l. If
potassium levels fall below 3.3 mmol/l,
insulin administration may need to be
interrupted to allow correction of the
hypokalemia.[1]

Bicarbonate

• The administration of sodium

bicarbonate solution to rapidly improve
the acid levels in the blood is
controversial. There is little evidence
that it improves outcomes beyond
standard therapy, and indeed some
evidence that while it may improve the
acidity of the blood, it may actually
worsen acidity inside the body's cells
and increase the risk of certain
complications. Its use is therefore
discouraged,[2][5][10] although some
guidelines recommend it for extreme
acidosis (pH<6.9), and smaller
amounts for severe acidosis (pH 6.9–
7.0).

Cerebral edema

• Cerebral edema, if associated with

coma, often necessitates admission to
intensive care, artificial ventilation, and
close observation. The administration
of fluids is slowed. The ideal treatment
of cerebral edema in DKA is not
established, but intravenous mannitol
and hypertonic saline (3%) are used—
 as in some other forms of cerebral
edema—in an attempt to reduce the
swelling.[2]

Resolution

• Resolution of DKA is defined as

general improvement in the symptoms,
such as the ability to tolerate oral
nutrition and fluids, normalization of
blood acidity (pH>7.3), and absence of
ketones in blood (<1 mmol/l) or urine.
Once this has been achieved, insulin
may be switched to the usual
subcutaneously administrered regimen,
one hour after which the intravenous
administration can be discontinued.
• In patients with suspected ketosis-
prone type 2 diabetes, determination of
antibodies against glutamic acid
decarboxylase and islet cells may aid
in the decision whether to continue
insulin administration long-term (if
antibodies are detected), or whether to
attempt treatment with oral medication
as in type 2 diabetes.

POSSIBLE COMPLICATIONS

• Fluid buildup in the brain (cerebral edema)

• Heart attack and death of bowel tissue due to low blood pressure
• Renal failure

PREVENTION

• People with diabetes should learn to recognize the early warning signs and symptoms of
ketoacidosis. In people with infections or who are on insulin pump therapy, measuring
urine ketones can give more information than glucose measurements alone.
• Insulin pump users need to check often to see that insulin is still flowing through the
tubing, and that there are no blockages, kinks, or disconnections.