Data Interpretation

Joshua Odendaal Flurina Michelotti

Contents
Arterial Blood Gases Anaemia Liver Function Tests

Arterial Blood Gases (ABG)

Site:
Radial Artery Brachial Artery Femoral Artery

Heparin:
Squirt out!!! Dilution effect

Air Bubbles:
Lead to false readings!

The Bodys Acid/Base System

Centres on the Bicarbonate Buffer System:

H+ + HCO3-

H2CO3

CO2 + H2O

Additional Buffer systems exist: including Haemoglobin and Phosphate systems

The Bodys Acid/Base System

Centres on the Bicarbonate Buffer System:

H+ + HCO3-

H2CO3

CO2 + H2O

Kidneys

Lungs

Problems

Metabolic Acidosis
Caused by:
Raised Hydrogen Ions Decreased secretion of Hydrogen Ions Decreased Bicarbonate production

H+ + HCO3-

H2CO3

CO2 + H2O

Compensation: Respiratory

 Causes: High Anion Gap

Lactic Acidosis Ketoacidosis Chronic Renal Failure Intoxication

Pattern: pH pCO2 HCO3 Compensated pH pCO2 HCO3-

Normal Anion Gap

Renal Tubular Acidosis Longstanding diarrhoea Pancreatic fistula

Respiratory Acidosis
Caused by:
Raised Carbon dioxide leading to raised hydrogen ions

H+ + HCO3-

H2CO3

CO2 + H2O

H+ + HCO3Compensation: Metabolic via kidneys

 Causes: Acute
Failure of Ventilation

Chronic
COPD Pickwickian Syndrome Neuromuscular conditions

Pattern: pH pCO2 HCO3 Compensated pH pCO2 HCO3-

Metabolic Alkalosis
Caused by: Decreased Hydrogen ions Increased Bicarbonate

H+ + HCO3-

H2CO3

CO2 + H2O

Compensation: Respiratory

 Causes:
Hypokalaemia Vomiting Pyloric Stenosis Ingestion of Bicarbonates

Pattern: pH pCO2 HCO3 Compensated pH pCO2 HCO3-

Respiratory Alkalosis
Caused by: Decreased Carbon dioxide leading to decreased hydrogen ions

H+ + HCO3-

H2CO3 H+ + HCO3Compensation: Metabolic

CO2 + H2O

 Causes:
Psychiatric Artificial Ventilation Stimulants

Pattern: pH pCO2 HCO3 Compensated pH pCO2 HCO3-

Type I Respiratory Failure

Characterized by:
Low oxygen Normal or low CO2 1 wrong

Caused by problems with oxygenation

Low Ambient Oxygenation Ventilation Perfusion Mismatch PE Impaired diffusion e.g. Pneumonia Acute asthma

Type II Respiratory Failure

Characterized by:
Low oxygen Raised CO2 2 wrong

Caused by:
Impaired ventilation COPD Neuromuscular conditions

Base Excess
Assesses the excess or deficit of base in the blood
Predominantly affected by serum bicarbonate Positive if too much base Negative if too little Useful as a means of confirming if a condition is metabolic If >+2 metabolic alkalosis If <-2 metabolic acidosis

Compensation
Beware compensation can confuse the picture
To fully assess compensation can calculate expected pH and if not as expected compensated!

[H+] = k x pCO2 [HCO3-]

Interpreting ABGs
1. Acidotic or Alkalotic 2. Respiratory or Metabolic
Different or same rule

3. Compensated?

1. 2. 3. 4.

Assess the patient Assess Oxygenation Determine the pH status Determine the respiratory component 5. Determine the metabolic component

Flenley Acid/Base Nomogram

Lets Practice!

Case 1
12 year old Diabetic patient with Kussmaul breathing ABG results:
pH pCO2: pO2: HCO3: BE: : 7.05 12 mmHg 108 mmHg 5 mEq/L -30 mEq/L

Diagnosis
Severe partially compensated metabolic acidosis without hypoxemia due to ketoacidosis

Case 2
17 year old Severe kyphoscoliosis Admitted for pneumonia ABG results:
pH: pCO2: pO2: HCO3: BE 7.37 25 mmHg 60 mmHg 14 mEq/L : -7 mEq/L

Diagnosis

Compensated respiratory acidosis due to chronic hypoventilation secondary to hypoxia

Case 3
9 year old History of asthma Audibly wheezing x 1 week, has not slept in 2 nights O/E: Using accessory muscles to breath, bilateral wheeze

ABG Result:
pH: pCO2: pO2 HCO3: BE: 7.51 2.0 mmHg 35 mmHg 22 mEq/L -2 mEq/L

Diagnosis

Uncompensated respiratory alkalosis with severe hypoxia due to asthma exacerbation

More Examples
1.PaO2 90 SaO2 2.PaO2 60 SaO2 3.PaO2 95 SaO2 4.PaO2 87 SaO2 5.PaO2 94 SaO2 6. PaO2 62 7.PaO2 93 SaO2 8.PaO2 95 SaO2 9.PaO2 65 SaO2 10. PaO2 110 95 90 100 94 99 SaO2 97 99 89 SaO2 pH 7.48 pH 7.32 pH 7.30 pH 7.38 pH 7.49 91 pH 7.35 pH 7.45 pH 7.31 pH 7.30 100 pH 7.48 PaCO2 32 HCO3 24 PaCO2 48 HCO3 25 PaCO2 40 HCO3 18 PaCO2 48 HCO3 28 PaCO2 40 HCO3 30 PaCO2 48 HCO3 27 PaCO2 47 HCO3 29 PaCO2 38 HCO3 15 PaCO2 50 HCO3 24 PaCO2 40 HCO3 30

Answers
1.Respiratory alkalosis 2.Respiratory acidosis 3.Metabolic acidosis 4.Compensated Respiratory acidosis 5.Metabolic alkalosis 6.Compensated Respiratory acidosis 7.Compensated Metabolic alkalosis 8.Metabolic acidosis 9.Respiratory acidosis 10.Metabolic alkalosis

Approaching the Anaemic Patient

Anaemia
Anaemia:
Hb <13.5 in males Hb <11.5 in females

Acute vs chronic
Acute features of shock Gradual onset:
Asymptomatic Fatigue, pallor Exertional dyspnoea, tachycardia, palpitaitons, angina, signs of cardiac failure

Approaching the Anaemic Patient

1) How severe is the anaemia? 2) How quickly treatment must be started is blood transfusion required?

3) Establish the cause of the anaemia

Causes
1. Defective production of RBC
Deficiency of iron, vitamin B12, folate Anaemia of chronic disease Reduced EPO in CKD Primary disease of bone marrow

2. Increased rate of loss of cells

Blood loss Haemolysis

Classification

MCV Low Normal High

= Microcytic

=Normocytic

=Macrocytic

Microcytic Anaemia
Ferritin

- Dietary - Gastritis - Chronic blood loss

- Anaemia of chronic disease ()

- Haemoglobinopathy

Iron Deficiency Anaemia (IDA)

Absorption in duodenum and upper part of jejenum Causes:
Reduced intake Increased demand Malabsorption Blood loss Infections

Bloods
FBC low Hb, low MCV, low ferritin Blood film microcytic, hypochromic, varied size (anisocytosis) and shape (poikilocytosis)

Management
Conservative diet Iron replacement PO or parenteral Packed red cell transfusion

Anaemia of Chronic Disease

Causes
Chronic infections Chronic inflammation Malignancy

Investigations FBC
Hb / MCV / ferritin

Management
Iron replacement PO or parenteral EPO injections Blood transfusions

Normocytic anaemia
Reticulocytes

-Anaemia of chronic disease - Renal failure - Bone marrow failure

- Haemoloysis - Blood loss

Macrocytic Anaemia
Vitamin B12 & Folate

-Haemolysis - Liver disease -Megaloblastic anaemia Hypothyroidism - Myeloma

- Alcohol excess
- Pregnancy

Megaloblastic Anaemia
Vit B12 deficiency Absorption in ileum via IF Reduced intake or impaired absorption Clinical features
Anaemia Peripheral neuropathy Weight loss Dementia Optic atrophy Can initially present with falls.

Folate defiency Absorption in jejenum Aetiology:

Reduced intake Malabsorption Coeliac, alcohol Increased demand malignancy, preganancy Increase loss liver disease Drugs anti-convulsants, metformin

Treatment IM hydroxycobalamin

Treatment 5mg folic acid OD

The Anaemic Patient

History
Symptoms Effect on life Try to identify the cause
Diet Drug history Gastrointestinal symptoms Weight loss Travel history Family history - ?thalasseamia

On Examination
Aim to establish:
Underlying cause Have any complications developed

General exmination
Pallor of mucous membranes Koilonychia Lymphadenopathy

GI ?intra-abdominal disease CVS - ?heart failure signs

Investigations
Bloods
FBC Reticulocytes Haematinics TFT LFTs Coeliac Screen CRP for IBD screen Myeloma screen

Blood film anisocytosis and poikilocytosis in IDA FOB Upper/lower GI endoscopy Bone marrow biopsy H.Pylori Screen

Approaching Abnormal Liver Function Tests (LFTs)

Liver Function Tests

Serum markers produced by the liver Measurement of liver function Assessment of jaundice Include:
Alanine Transaminase (AST) Aspartate Transaminase (ALT) Alkaline Phosphatase (ALP) Albumin Bilirubin Clotting factors Alpha-fetoprotein

LFTs
Serum Markers of Liver Function
ALT AST ALP GGT

Markers of Synthetic Function

Albumin PT/INR

Help locate area of damage!

Bilirubin

AFP tumour marker

ALT and AST

Enyzmes contained within cytoplasm of hepatocytes Elevated when hepatocytes die Small amount present in other organs ALT more specific for hepatic damage
Viral or drug induced hepatitis

AST rises more in alcohol and cirrhosis

Levels fluctuate according to amount of acute damage Useful for monitoring liver damage and regeneration

GGT
In hepatocytes and epithelium of bile ducts Elevation in:
Chronic alchohol use Bile duct disease Hepatic metastases

ALP
Enzyme in cells lining the biliary ducts Elevation in:
Extra hepatic bile duct obstruction Intrahepatic cholestasis Malignancy

Also present in bone and placenta

Albumin
Main protein synthesised by liver Contributes to oncotic pressure and transport of nutritents/drugs Levels are decresed in :
Low production chronic liver disease, malnutirtion Loss GI, renal Sepsis

Bilirubin
Elevated levels jaundice Hepatocytes take up unconjugated bilirubin, conjugate and excrete it Jaundice can be:
Pre-hepatic heamolysis Hepatic hepatitis, genetic, drug reaction Post hepatic bile duct obstruction, drugs
Pre-Hepatic Hepatic Post-Hepatic Unconjugated Bilirubin +++ ++ Conjugated Bilirubin ++ +++

A Simple Approach to Deranged LFTs

Jaundice

bilirubin enzymes

ALP

ALT and AST

- Haamolysis - Gilberts syndrome

USS - ?duct dilation - No drugs, PBC, PSC - Yes obstruction from gallsotones or malignancy

Hepatocellular damage acute/Chronic

Pattern of LFT Damage

1. Obstructive
bilirubin ALP ALT

2. Hepatic
ALT Varying bilirubin the higher, the greater the level of damage Slight ALP PT/INR

Other Tests used in Diagnosis

Non-Invasive Liver Screen (NILS)
Viral serology Hep screen, HIV, CMV, EBV Auto-antibodies ANA, AMA Iron studies Copper studies AFP

USS ERCP Histopathology

The Patient with Abnormal LFTs

History
Symptoms jaundice Drug history Alcohol Recent foreign travel Blood transfusions Unprotected sexual intercourse DM, obesity, hyperlipidaemia fatty liver Fatty liver

The Patient with Abnormal LFTs

Examination
Stigmata of chronic liver disease
Jaundice Palmar erythema Bruising Spider naevi Gyneacomastia

Hepatomegally Splenomegally Ascites Obesity Features of hepatic encephelopathy

Scenarios

Case 1
24, M Student PC yellowing of sclera after an end of term party No PMH SH binge drinker, nil drug use DH nil Normal examination

Investigations
Bilirubin Albumin ALT 36 40 35 (<17umol/L) (35-51 g/L) (<40 U/L)

AST
ALP GGT

36
86 35

(<40 U/L)
(35-51 U/L) (11-42 U/L)

Diagnosis
Elevated bilirubin - ?conjugated or unconjugated Urine no bilirubin or urobilogen
Therefore the cause is pre-hepatic

No increase in reticulocytes therefore not haemolysis

Gilberts syndrome harmless!

Case 2
38, F PC jaundice, itch, dark urine PMH UTI a week ago, treated with antibiotics by GP SH 21 units/week, smokes 15/day O/E no signs of chronic liver disease

Investigations
Bilirubin Albumin ALT 236 38 65 (<17umol/L) (35-51 g/L) (<40U/L)

AST
ALP GGT

55
1024 59

(<40U/L)
(35-51 U/L) (11-42 U/L)

Diagnosis
USS no bile duct obstruction Drug induced cholestasis secondary to co-amoxiclav Self-limiting jaundice resolved over 3 weeks

Case 3
18, F Returned from India 1 week ago PC unwell for the past 10 days with diarrhoea, fevers, joint pain and in the last 2 days has turned yellow Took some tablets in a night club and had a small tattoo done PM nil DH anti-malarials O/E jaundice, no signs of chronic liver disease

Investigations
Bilirubin Albumin ALT 168 38 2500 (<17umol/L) (35-51 g/L) (<40U/L)

AST
ALP GGT

2380
190 39

(<40U/L)
(35-51 U/L) (11-42 U/L)

Diagnosis
Further investigations
USS no duct dilation. Swollen liver Serum IGM anti-HAV positive

Acute hepatits A

Case 4
19, F student Recently failed exams and split up with boyfriend PC vomiting Overdose of 32g of paracetamol with alcohol PMH nil DH nil

Investigations
Bilirubin Albumin ALT 25 40 5500 (<17umol/L) (35-51 g/L) (<40U/L)

AST
ALP GGT

3400
200 450

(<40U/L)
(35-51 U/L) (11-42 U/L)

INR

2.8

Diagnosis
Acute liver failure due to paracetamol overdose Treated with N-acetylcysteine For liver transplant

Managing Deranged U&Es

Example
Potassium 4.3 mmol/L 3.5-5.3

Sodium
eGFR Urea Creatinine

142 mmol/L
23 14.6 mmol/L 246 umol/L

133-146

2.5-7.8 64-104

Questions in Assessing
1. Is it new?
If Yes as per next slide If No..

2. Is it stable?
If No as per next slide If Yes continue to monitor bloods, particularly K. Consider supplementing with fluids

If the Onset is Acute (AKI or AKI on CKD)

Pre-Renal History Blood loss trauma, surgery PMH Drugs Renal Vasculitis Autoimmune disease Recent infection DM, HTN Post-Renal Stones Urinary symptoms BPH Weight loss

Symptoms

Confusion Oliguria/anuria
Dehydration Septic Fluid resuscitation

Oliguria/anuria Fluid overload

Oliguria/Anuria Dysuria Haeaturia

On Examination

Small fibrotic kidneys Palpable bladder Systemic signs Avoid nephrotoxic drugs BP control Catheter

Management

Key Management Principles

1. Treat underlying cause
2. Treat Complications Acidosis IV sodium bicarbonate Hyperkalaemia Uraemia dialysis Dehydration fluids!!!!! Pulmonary oedema IV furosemide 3. Supportive

Hyperkalaemia
SEVERE - K+ 7.0 mmol/L Presence of symptoms - Muscle weakness, paralysis, palpitations and paraesthesias ECG changes MODERATE - K+ 6.1 - 7.0 mmol/L no symptoms or ECG changes MILD - K+ 5.1 - 6.0 mmol/L asymptomatic

ECG Changes

Small/absent P waves

Broad QRS

Slurring into ST segment Tall tented T waves

Long PR interval

Management
ECG and drug chart IV 10mL of 10% Ca gluconate 50mLs of 20% dextrose with 10 units Actrapid Salbutamol nebulisers

Calcium resonium

Summary!

Any Questions?

Reassure likely to be Gilberts Syndrome gamma-GT only From history: - Alcohol? - Enzyme inducing drugs? - Obese? Reduce alcohol intake No action Lose weight ALP / ALT <2x normal ----------------------------------------------Reduce alcohol intake Stop hepatotoxic drugs Lose Weight (BMI>25) Recheck LFTs in 3-6 months ALP / ALT >2x normal (or <2x normal, but persistently high) Further Tests: - Hepatitis virus - Autoimmune tests - Ferritin - USS liver Dilated bile ducts: - Cholangiography, ERCP Normal bile ducts:

Example 1
AST ALT ALP Bilirubin Ablumin 95 88 85 21 41 27 18 98 49 43 1218 1055 191 140 31 104 114 390 87 39