Data Interpretation MUHAMMAD MUJAMMAMI, MD, MSc, ECNU, FACE, SEAP – Endo Cert. Assistant Professor of Medicine, College of Medicine, King Saud University.

Data Interpretation MUHAMMAD MUJAMMAMI, MD, MSc, ECNU, FACE, SEAP – Endo Cert. Assistant Professor of Medicine, College of Medicine, King Saud University Consultant in Medicine, Endocrinology, Thyroid & Neuroendocrine Oncology, KSUMC October 2019

Chest X-ray

Normally the pleural space contains: 3.5 to 7.0 ml of clear liquid
PLEURAL EFFUSION Normally the pleural space contains: 3.5 to 7.0 ml of clear liquid low protein content small number of mononuclear cells Pleural effusion: presence of large amount of fluid in the pleural space irrespective of the underlying causes

Indication for Pleural Fluid Analysis
PLEURAL EFFUSION Indication for Pleural Fluid Analysis Diagnostic ( detect underlying diagnosis) Therapeutic (relief shortness of breath)

Transudates vs Exudates
LIGHT’S CRITERIA* 1. Pleural Protein divided by serum protein >0.5 2. Pleural fluid LDH divided by Serum LDH >0.6 3. Pleural fluid LDH > 2/3 the upper limit of normal for the serum LDH.

Constrictive Pericarditis Pulmonary Infarction Hypothyroidism
Causes of Transudates and Exudates Tronsudote Exudate Left Heart Failure Bacterial Pneumonia Carcinoma Bronchus Hypoproteinaemia Constrictive Pericarditis Pulmonary Infarction Hypothyroidism Cirrhosis Connective-tissue Disease Tuberculosis

CELL COUNT PLEURAL EFFUSION
Transudate < 1000 but 20% > 1000 and rarely > 10,000/mm3 Exudate > 1000/mm3 Limited value (unless > 50,000/mm3  emphyema)

PF LYMPHOCYTE-PREDOMINANT EXUDATES (>80%)
PLEURAL EFFUSION PF LYMPHOCYTE-PREDOMINANT EXUDATES (>80%) Causes TB Lymphoma `Chronic lymphocytic leukaemia

BIOCHEMISTY PLEURAL EFFUSION
Glucose < 3.3 mmol/L or 1/2 serum glucose (simultaneous) - Rheumatoid pleurisy (85%) - Empyema (80%) - Malignancy (40%)

BIOCHEMISTY PLEURAL EFFUSION Pleural fluid pH:
- Normal pleural fluid pH is > 7.6 - Transudates – pH - Exudates – pH is Should always be measured in a blood gas machine Parapneumonic - pH < 7.0 predicts “complicated effusion” that is unlikely to resolve without chest tube drainage. Malignant effusion with a pH < 7.3 is associated with poor survival. If pH < 6.0 think of ruptured esophagus

positive in about 60% of patients with malignant effusion
PLEURAL EFFUSION CYTOLOGY positive in about 60% of patients with malignant effusion

PLEURAL EFFUSION Patients with Abnormal Chest Radiograph
Suspect pleural disease Blunting of costophrenic angle? YES Lateral decubitus chest radiographs Yes No Diagnostic thoracentesis Fluid thickness > 10mm Observe

PLEURAL EFFUSION SUMMARY Yes No Diagnostic thoracentesis
Any of the following met? PF/serum protein >0.5 PF/serum LDH >0.6 PF LDH >2/3 upper normal Serum limit Yes No Exudate Transudate Appearance of plueral fluid, pH & glucose, cytology and differential cell count of pleural fluid Treat CHF, cirrhosis, or nephrosis

Ascites Arthur Harris, MD Attending, Division of Gastroenterology
Jacobi Medical Center/North Central Bronx Hospital Assistant Professor of Medicine, AECOM

Ascites – Patient Evaluation
Assess liver function Evaluation of renal and CVS function Ascitic fluid analysis Endoscopy for varices

It’s all about the sodium
Therapy It’s all about the sodium

ATERIAL BLOOD GASES

DEFINITION It is a diagnostic procedure in which a blood is obtained from an artery directly by an arterial puncture or accessed by a way of indwelling arterial catheter A.Y.T

ABG component PH: measures hydrogen ion concentration in the blood, it shows blood’ acidity or alkalinity PCO2 : It is the partial pressure of CO2 that is carried by the blood for excretion by the lungs, known as respiratory parameter PO2: It is the partial pressure of O2 that is dissolved in the blood , it reflects the body ability to pick up oxygen from the lungs HCO3 : known as the metabolic parameter, it reflects the kidney’s ability to retain and excrete bicarbonate A .Y .T

Normal values: PH = (7.35 – 7.45) PCO2 = 40 (35 – 45) Acid - Respiratory PO2 = – 100 mmhg HCO3 = 24 (22 – 28) meq/L Alkaline - Metabolic

Interpretation of ABG results
PH acidemia PaCO mmhg increased (respiratory cause) HCO meq/l normal PaO mmhg normal Respiratory acidosis PH alkalemia PaCO mmhg normal HCO meq/l increased (metabolic cause) PaO mmhg normal Metabolic alkalosis A.Y.T

Acid base disorders Respiratory acidosis PH ↓ PCO2 ↑ HCO3 ------ A.Y.T

Respiratory alkalosis
PH ↑ PCO2 ↓ HCO3 ------ A.Y.T

Metabolic acidosis PH ↓ PCO2 ------ HCO3
A.Y.T

Metabolic alkalosis PH ↑ PCO2 ------ HCO3
A.Y.T

Compensation The respiratory and metabolic system works together to keep the body’s acid-base balance within normal limits. The respiratory system responds to metabolic based PH imbalances in the following manner: * metabolic acidosis: ↑ respiratory rate and depth (↓PaCO2) * metabolic alkalosis: ↓ respiratory rate and depth (↑PaCO2) The metabolic system responds to respiratory based PH imbalances in the following manner: *respiratory acidosis: ↑ HCO3 reabsorption *respiratory alkalosis: ↓HCO3 reabsorption A.Y.T

a. Respiratory acidosis
Phase PH PaCO2 HCO3 UNCOMPENSATED ↓ ↑ ------ Because there is no response from the kidneys yet to acidosis the HCO3 will remain normal Phase PH PaCO2 HCO3 PARTIAL COMPENSATED ↓ ↑ The kidneys start to respond to the acidosis by increasing the amount of circulating HCO3 Phase PH PaCO2 HCO3 FULL COMPENSATED N ↑ PH return to normal PaCO2 & HCO3 levels are still high to correct acidosis A.Y.T

B. Respiratory alkalosis
Phase PH PaCO2 HCO3 UNCOMPENSATED ↑ ↓ ------ Because there is no response from the kidneys yet to acidosis the HCO3 will remain normal Phase PH PaCO2 HCO3 PARTIAL COMPENSATED ↑ ↓ The kidneys start to respond to the alkalosis by decreasing the amount of circulating HCO3 Phase PH PaCO2 HCO3 FULL COMPENSATED N ↓ PH return to normal PaCO2 & HCO3 levels are still low to correct alkalosis A.Y.T

C. Metabolic acidosis Phase PH PaCO2 HCO3 UNCOMPENSATED ↓ Because there is no response from the lungs yet to acidosis the PaCO2 will remain normal Phase PH PaCO2 HCO3 PARTIAL COMPENSATED ↓ The lungs start to respond to the acidosis by decreasing the amount of circulating PaCO2 Phase PH PaCO2 HCO3 FULL COMPENSATED N ↓ PH return to normal PaCO2 & HCO3 levels are still low to correct acidosis A.Y.T

D. Metabolic alkalosis Phase PH PaCO2 HCO3 UNCOMPENSATED ↑ Because there is no response from the lungs yet to alkalosis the PaCO2 will remain normal Phase PH PaCO2 HCO3 PARTIAL COMPENSATED ↑ The lungs start to respond to the alkalosis by increasing the amount of circulating PaCO2 Phase PH PaCO2 HCO3 FULL COMPENSATED N ↑ PH return to normal PaCO2 & HCO3 levels are still high to correct alkalosis A.Y.T

tutorial Example 1 XX is a 45-year-old female admitted with a severe asthma attack. She has been experiencing increasing shortness of breath since admission three hours ago Her arterial blood gas result is as follows Clinical Laboratory: pH 7.22 PaCO2 55 HCO3 25 Follow the steps: 1. Assess the pH. It is low therefore, we have acidosis. 2. Assess the PaCO2. It is high and in the opposite direction of the pH. 3. Assess the HCO3. It has remained within the normal range (22-26). Acidosis is present (decreased pH) with the PaCO2being increased, reflecting a primary respiratory problem. For this patient, we need to improve the ventilation status by providing oxygen therapy, mechanical ventilation or by administering bronchodilators. A.Y.T

Follow the steps again:
Example 2 XY is a 55-year-old male admitted with a recurring bowel obstruction. He has been experiencing intractable vomiting for the last several hours, Here is his arterial blood gas result: Clinical Laboratory: pH 7.50 PaCO2 42 HCO3 33 Follow the steps again: 1. Assess the pH. It is high (normal ), therefore, indicating alkalosis. 2. Assess the PaCO2. It is within the normal range (normal 35-45). 3. Assess the HCO3. It is high (normal 22-26) and moving in the same direction as the pH. Alkalosis is present (increased pH) with the HCO3 increased, reflecting a primary metabolic problem. Treatment of this patient might include administration of I.V. fluids and measures to reduce the excess base. A.Y.T

The Terms ACIDS BASES Acidemia Acidosis Alkalemia Alkalosis
Respiratory CO2 Metabolic HCO3 BASES Alkalemia Alkalosis Respiratory CO2 Metabolic HCO3

Respiratory Acidosis ph, CO2, Ventilation Causes CNS depression
Pleural disease COPD/ARDS Musculoskeletal disorders Compensation for metabolic alkalosis

Respiratory Alkalosis
pH, CO2, Ventilation  CO2   HCO3 (Cl to balance charges  hyperchloremia) Causes CHAMPS C – CNS Disease e.g. Intracerebral hemorrhage/ Cirrhosis H – Hypoxia A – Anxiety M – Over ventilation P – Progesterone S – Salicylate/Sepsis

Metabolic Acidosis pH, HCO3
12-24 hours for complete activation of respiratory compensation The degree of compensation is assessed via the Winter’s Formula  PCO2 = {1.5(HCO3) +8  2 } x [converts to kPa]

The Causes Metabolic Gap Acidosis Non Gap Metabolic Acidosis
M - Methanol U - Uremia D – DKA - AKA P - Paraldehyde I – Isoniazid / Iron L - Lactic Acidosis E - Ethylene Glycol R- Rhabdomyolysis S - Salicylate Non Gap Metabolic Acidosis H - Hyperalimentation A - Acetazolamide R - RTA D - Diarrhoea U - Uretero-pelvic shunt P - Pancreatic Fistula S – Spironolactone

Metabolic Alkalosis pH, HCO3 Causes – CLEVER PD C- Contraction
L - Liquorice E - Endocrine: Conn’s / Cushing’s / Bartter’s V - Vomiting / NG Suction E - Excess Alkali R - Refeeding Alkalosis P - Post Hyper-capnoea D - Diuretics and Chronic diarrhoea

Liver Function Tests (LFTs)

Liver Function Tests (LFTs)
Broadly classified as: Tests to detect hepatic injury: Mild or severe; acute or chronic Nature of liver injury (hepatocellular or cholestasis) Tests to assess hepatic function

Classification of LFTs
Group I: Markers of liver dysfunction Serum bilirubin: total and conjugated Urine: bile salts and urobilinogen Total protein, serum albumin and albumin/globulin ratio Prothrombin Time

Group II: Markers of hepatocellular injury Alanine aminotransferase (ALT) Aspartate aminotransferase (AST)

Group III: Markers of cholestasis Alkaline phosphatase (ALP) g-glutamyltransferase (GGT)

Limitations of LFTs Normal LFT values do not always indicate absence of liver disease Liver a has very large reserve capacity Asymptomatic people may have abnormal LFT results Diagnosis should be based on clinical examination

Common serum liver chemistry tests

Bilirubin A byproduct of red blood cell breakdown
It is the yellowish pigment observed in jaundice High bilirubin levels are observed in: Gallstones, acute and chronic hepatitis

Serum bilirubin levels
Normal 0.2 – 0.8 mg/dL Unconjugated (indirect): 0.2 – 0.7 mg/dL Conjugated (direct): Must be < 50% of Total 0.1 – 0.4 mg/dL Latent jaundice: Above 1 mg/dL Jaundice: Above 2 mg/dL

Bilirubin levels and jaundice
Class of Jaundice Causes Pre-hepatic or hemolytic Abnormal red cells; antibodies; drugs and toxins; thalessemia Hemoglobinopathies, Gilbert’s, Crigler-Najjar syndrome Hepatic or Hepatocellular Viral hepatitis, toxic hepatitis, intrahepatic cholestasis Post-hepatic Extrahepatic cholestasis; gallstones; tumors of the bile duct, carcinoma of pancreas

Serum Albumin The most abundant protein synthesized by the liver
Normal serum levels: 3.5 – 5 g/dL Synthesis depends on the extent of functioning liver cell mass Longer half-life: 20 days Its levels decrease in all chronic liver diseases

Prothrombin Time (PT) Prothrombin: synthesized by the liver, a marker of liver function Half-life: 6 hrs. (indicates the present function of the liver) PT is prolonged only when liver loses more than 80% of its reserve capacity Vitamin K deficiency also causes prolonged PT Intake of vitamin K does not affect PT in liver disease

Aspartate aminotransferase (AST)
Normal range: 8 – 20 U/L A marker of hepatocellular damage High serum levels are observed in: Chronic hepatitis, cirrhosis and liver cancer

Alanine aminotransferase (ALT)
More liver-specific than AST Normal range (U/L): Male: 13-35 Female: 10-30 High serum levels in acute hepatitis ( U/L) Moderate elevation in alcoholic hepatitis ( U/L) Minor elevation in cirrhosis, hepatitis C and non-alcoholic steatohepatitis (NASH) (50-100U/L)

Alanine aminotransferase (ALT)
Appears in plasma many days before clinical signs appear A normal value does not always indicate absence of liver damage Obese but otherwise normal individuals may have elevated ALT levels

Alkaline phosphatase (ALP)
A non-specific marker of liver disease Produced by bone osteoblasts (for bone calcification) Present on hepatocyte membrane Normal range: 40 – 125 U/L Modearte elevation observed in: Infective hepatitis, alcoholic hepatitis and hepatocellular carcinoma

Alkaline phosphatase (ALP)
High levels are observed in: Extrahepatic obstruction (obstructive jaundice) and intrahepatic cholestasis Very high levels are observed in: Bone diseases

g-glutamyltransferase (GGT)
Used for glutathione synthesis Normal range: 10 – 30U/L Moderate elevation observed in: Infective hepatitis and prostate cancers GGT is increased in alcoholics despite normal liver function tests Highly sensitive to detecting alcohol abuse

Take Home Messages LFTs help detect liver injury and function.
LFTs do have some limitations.

Thyroid Function Test

1 2 3 4 5 6 7 T4 Normal Low High TSH Low/ normal High/normal
Investigation No ? TPO Abs MRI Pituitary hormones Thyroid scan Diagnosis Eu-thyroid Primary Hypo-thyroid Secondary Thyrotoxicosis Hyper-thyroid Subclinical Hypothyroid Hyperthyroid Treatment Thyroxine B-Blocker Anti-thyroid Rx (if hyperthyroid) Surgery Anti-thyroid No Rx unless: TSH> 10 Pregnant + positive TPO Abs 65 years AF Osteoporosis

Calcium Metabolism

PTH Normal High Low Calcium Vitamin D Diagnosis Vitamin D deficiency Hypocalcemia Hypoparathyroidism PTH-dependent hypercalcemia Such as Primary hyperparathyroidism Non-PTH dependent Investigation No NO Urine Ca/Cr ratio Parathyroid scan R/O malignancy & other causes Treatment replacement Replacement (active) IV fluid Calcitonin Bisphosphonate Surgery Treat the cause

Anemia

Complete Blood Count < leukopenia > Leukocytosis

Leukocytosis? Which cell line?
Neutrophilia  Acute: bacterial infection, steroids. Chronic: Chronic myeloid leukemia (CML) Lymphocytosis  Acute: viral infections Chronic: chronic lymphocytic leukemia Monocytosis  fungal infection, TB Eosinophilia  allergic conditions, parasite, autoimmune diseases and eosinophilic leukemia Basophilia  very rare, CML

Leukopenia? Which cell line? What degree?
Neutropenia: Mild: Absolute neutrophilic count (ANC)  Moderate: ANC  Severe: ANC  < 0.5 Risk of infection not increased no need to investigate Risk of infection is increased. Must investigate Risk of infection not increased. But need to investigate

7 Complete Blood Count

Measures the absolute RBC count:
7 Complete Blood Count Measures the absolute RBC count: 1- Low 2- Normal 3- High

7 Complete Blood Count Low  anemia High  polycythemia

Complete Blood Count Low  microcytic Normal  normocytic
7 Complete Blood Count Low  microcytic Normal  normocytic High  macrocytic

7 Complete Blood Count Low  hypochromic Normal  normochromic

High  hereditary spherocytosis
7 Complete Blood Count High  hereditary spherocytosis

Complete Blood Count High  high variation in RBC sizes (anisocytosis)
7 Complete Blood Count High  high variation in RBC sizes (anisocytosis) Normal/Low  low or no variation in sizes

Approach to anemia To start your approach with any case of anemia you need to look at three CBC parameters and one additional test. The 3 CBC parameters are: The hemoglobin (Hb) MCV and Reticulocyte count (retic count). And the additional required test is the peripheral blood smear.

Approach to anemia With the use of these 3 parameters your approach will be divided into 4 categories. Low MCV (MCV < 80 fL), also called microcytic anemia. Normal MCV (MCV fL) with low retic count, also called normocytic anemia with inappropriately low bone marrow response. Normal MCV (MCV fL) with high retic count, also called normocytic anemia with appropriate marrow response. High MCV (MVC >100 fL), also called macrocytic anemia.

Iron deficiency or thalsemia
MCV < 80 fL (TAILS) MCV N, low retic count MCV N, high retic count MCV > 100 fL 1) Thalassemia 2) Anemia of inflammation 3) Iron deficiency 4) Lead poisoning 5) Sideroblastic anemia Bone marrow failure: Aplastic anemia 2) BM suppression: - Toxins, sepsis. - Organ failure: renal failure, liver failure, adrenal insufficiency Chronic inflammation chronic diseases 3) BM infiltration: - Lymphoma, leukemia metastatic solid tumour granulomatous disease (e.g. TB) 1) bleeding 2) hemolysis 3) treated nutritional deficiency 1) Megaloblastic: (impaired nucleic acid metabolism): - B12 deficiency - folate deficiency - drugs: such as methotrexate 2) Non megaloblastic: - liver disease - alcohol - Myelodysplasia - thyroid disease - myeloma - Congenital bone marrow failure syndromes Iron deficiency or thalsemia

Microcytic anemia Iron deficiency anemia vs thalassemia.
Both will have low Hb and low MCV. How to differentiate? Iron deficiency anemia Thalassemia MCV Low (80-70s) Very low (70-60s) RBC Low High or normal RDW High normal Ferritin/iron level

Data Interpretation MUHAMMAD MUJAMMAMI, MD, MSc, ECNU, FACE, SEAP – Endo Cert. Assistant Professor of Medicine, College of Medicine, King Saud University.

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Data Interpretation MUHAMMAD MUJAMMAMI, MD, MSc, ECNU, FACE, SEAP – Endo Cert. Assistant Professor of Medicine, College of Medicine, King Saud University.

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