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Urinalysis & Body Fluids

Disease Correlation

We have reached the culmination of our study of serous fluids. We’ve learned the physiology, the importance of handling, and the specifics of physical, chemical, and microscopic testing. Today, we put on our clinical consultant hats. Our job is no longer just to generate results but to interpret the pattern of those results to paint a clear picture of the patient’s disease state

An effusion is a symptom, not a diagnosis. The fluid itself holds the clues to the underlying cause. Let’s examine the classic laboratory profiles of the most common and critical diseases that cause serous fluid effusions

Scenario 1: The Transudative Effusion

The first and most important branch point is the classification of the fluid as a transudate. If our results point in this direction, the clinical focus immediately shifts from local disease to systemic disease

Congestive Heart Failure (CHF)

  • Pathophysiology: The heart’s failure as a pump leads to increased systemic venous pressure. This elevates the hydrostatic pressure in the pleural capillaries, overwhelming the normal reabsorptive and lymphatic drainage capacity
  • The Classic Laboratory Profile
    • Classification: Transudate. (Fails all of Light’s criteria; SAAG would be ≥1.1 if peritoneal)
    • Appearance: Clear, pale yellow (serous)
    • WBC Count: Low (< 1000/µL)
    • Differential: A mix of lymphocytes, macrophages, and mesothelial cells. No single cell type predominates
    • Chemistry: Protein and LDH are low. Glucose is normal
  • Clinical Pearl: Sometimes, aggressive diuresis can concentrate a transudative pleural effusion, causing its protein level to rise and falsely meet exudative criteria (“pseudoexudate”). In these cases, the serum-fluid albumin gradient can be helpful. A gradient > 1.2 g/dL suggests the effusion is still a transudate from CHF

Cirrhosis

  • Pathophysiology: Severe liver scarring leads to two problems: 1) Portal Hypertension, which drastically increases hydrostatic pressure in the peritoneal capillaries, and 2) Impaired Albumin Synthesis, which lowers the plasma oncotic pressure. Both mechanisms strongly favor the formation of ascites
  • The Classic Laboratory Profile (Peritoneal Fluid/Ascites)
    • Classification: Transudate. The key finding is a SAAG ≥ 1.1 g/dL.
    • Appearance: Clear, pale yellow
    • WBC Count: Very low (< 250/µL)
    • Protein: Very low, often < 1.0 g/dL
  • A Critical Complication: Spontaneous Bacterial Peritonitis (SBP).: Patients with cirrhotic ascites are at high risk for developing SBP. The lab profile changes dramatically:
    • Appearance: Becomes turbid/cloudy
    • WBC Count: Jumps to > 250/µL
    • Differential: A neutrophil count > 50% of the total WBCs
    • This is a medical emergency requiring immediate antibiotic treatment

Scenario 2: The Exudative Effusion - Infection

If the fluid is an exudate, the hunt for a local cause begins. Infection is a primary concern

Parapneumonic Effusion & Empyema (Pleural Fluid)

  • Pathophysiology: An infection in the adjacent lung tissue (pneumonia) causes a localized inflammatory response in the pleura. This can progress from a simple sterile effusion to a complicated effusion with bacterial invasion, and finally to an empyema (frank pus in the pleural space)
  • The Classic Laboratory Profile
    • Classification: Exudate. (Meets Light’s criteria)
    • Appearance: Turbid to purulent
    • WBC Count: High (>10,000/µL), often >50,000/µL in empyema
    • Differential: Marked Neutrophilia (>75%).
    • Chemistry: Low Glucose (<60 mg/dL) and Low pH (<7.2) are critical markers of a complicated effusion/empyema that requires drainage
    • Microbiology: Gram stain and culture may be positive

Tuberculosis (TB)

  • Pathophysiology: A delayed-type hypersensitivity reaction to mycobacterial antigens in the pleural or peritoneal space. The response is T-cell mediated, not a neutrophilic one
  • The Classic Laboratory Profile
    • Classification: Exudate.
    • Appearance: Serous to serosanguinous (bloody-tinged), may form a web-like clot
    • WBC Count: Moderately high (1,000-5,000/µL)
    • Differential: Lymphocyte Predominance (>75%). This is the key cellular finding. Mesothelial cells are often conspicuously absent
    • Chemistry: Protein is very high. Glucose is often low
    • The “Telltale” Marker: Adenosine Deaminase (ADA).: An elevated ADA level (>40 U/L) is a highly sensitive and specific marker for tuberculous effusions
    • Microbiology: AFB stain is rarely positive; culture or PCR is required

Scenario 3: The Exudative Effusion - Malignancy

Cancer is one of the most common causes of exudative effusions, especially in older adults

  • Pathophysiology: Tumor cells can directly seed the serous surfaces, causing fluid production. They can also obstruct lymphatic drainage, causing fluid to back up
  • The Classic Laboratory Profile
    • Classification: Exudate.
    • Appearance: Can be serous, but is often hemorrhagic (bloody)
    • WBC Count: Highly variable
    • Differential: Often a lymphocytic predominance (the host’s immune response to the tumor), but the key is the search for the malignant cells themselves
    • Chemistry: Glucose can be low due to tumor metabolism
    • Definitive Diagnosis: Cytology.: The identification of malignant cells with their characteristic abnormal features is the only way to definitively diagnose a malignant effusion. This is the gold standard

Scenario 4: Other Important Exudates

Pancreatitis

  • Pathophysiology: Inflammation of the pancreas allows enzyme-rich pancreatic fluid to leak and track into the peritoneal or pleural cavities (usually the left side), causing intense chemical inflammation
  • The Classic Laboratory Profile
    • Classification: Exudate.
    • Appearance: Often serosanguinous or turbid
    • The Key Finding: Markedly Elevated Amylase (and Lipase).: The fluid amylase level will be significantly higher than the simultaneous serum level

Chylothorax

  • Pathophysiology: Disruption of the thoracic duct due to trauma or tumor, leading to the leakage of chyle (lymphatic fluid rich in dietary triglycerides) into the pleural space
  • The Classic Laboratory Profile
    • Appearance: Milky white and opaque.
    • Differential: Lymphocyte predominance (chyle is a lymphatic fluid)
    • The Key Finding: Triglyceride Level > 110 mg/dL.: This is diagnostic

Conclusion: The Power of Pattern Recognition

As we’ve seen, no single test result makes a diagnosis. A high lymphocyte count could be TB or cancer. Low glucose could be infection or malignancy. It is the constellation of findings - the appearance, the cell counts, the key chemical markers, and the cellular morphology - that allows us to pinpoint the underlying disease. Our final laboratory report is more than a list of data; it is a synthesized, expert interpretation that guides the clinician to the correct diagnosis and, ultimately, to the correct treatment for the patient. This is the apex of our role in the analysis of serous fluids