Fluid Analysis

A systematic approach to the analysis of the fluid in conjunction with the clinical presentation helps to understand the etiology, narrow the differential diagnoses, & design a management plan. Includes biochemistry, microscopic examinations & infectious disease tests.

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Myasthenia gravis

 

 Chronic, constantly progressive disease. Initially, it affects the muscle tissues of the face, then spreads to the trunk. The following types of MG are distinguished:

• Ocular – the nerve endings in the cranial region are affected, and the eyelids fall asymmetrically. The patient complains of double vision and deterioration in visual acuity. Gradually focusing on one subject becomes difficult.
• Bulbar – the lesion extends to the masticatory muscles and tissues of the larynx. The patient’s voice changes, speech becomes quieter and nasal. Some consonants are very difficult to pronounce, and stuttering develops. Due to the penetration of fluid into the respiratory tract, the risk of pneumonia increases.
• Lambert-Eaton – the muscles of the arms, legs, and neck do not receive nerve impulses. It is difficult for the patient to coordinate these areas of the body. This form is diagnosed in the elderly and is characterized by rapid progression.
• Generalized – the muscles of the eyes are immediately affected, then the process spreads to the larynx, arms, legs, and hips. The main danger of this form is that the respiratory muscles are affected over time.

The disease is characterized by constant progression. 

Plasma exchange (PLEX) is first-line for severe exacerbation & usually causes improvement in a few days. It directly removes anti-acetylcholine receptor antibody from the body. May be more effective in MuSK+ patients.

IVIG may be useful for less severe exacerbations; takes longer to work (e.g., 2-3 weeks), but the efficacy may be more sustained. The dose of IVIG is 2 grams/kg, usually divided over 2 or 5 days.

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Drug-induced thrombocytopenia

Immune-mediated: Certain drugs can trigger an immune response that leads to the production of antibodies targeting and destroying platelets. This immune-mediated destruction is a common mechanism of drug-induced thrombocytopenia (DITP). Examples of drugs associated with immune-mediated DITP include specific antibiotics (e.g., penicillins and sulfonamides), nonsteroidal anti-inflammatory drugs (NSAIDs), and some anticonvulsants.

Non-immune-mediated: Other drugs can cause thrombocytopenia through non-immune mechanisms, such as direct toxicity to the bone marrow, where platelets are produced. For instance, chemotherapeutic agents can suppress bone marrow function, resulting in decreased platelet production.

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Mean Arterial Pressure (MAP)

Average arterial pressure throughout one cardiac cycle, systole, and diastole. 

Surrogate indicator of blood flow and believed to be a better indicator of tissue perfusion.

To perfuse vital organs requires the maintenance of a minimum MAP of 60 mmHg. 

MAP = [Cardiac Output (CO) x Systemic Vascular Resistance (SVR)] + Central Venous Pressure (CVP)

MAP = (CO × SVR) + CVP

Because CVP is usually at or near 0 mmHg, this relationship is often simplified to:

MAP ≈ CO × SVR.

Cardiac output (CO) = Heart Rate (HR) X Stroke Volume (SV).

Stroke Volume is by ventricular inotropy and preload. 

Preload is affected by blood volume and the compliance of veins. 

Increasing the blood volume increases the preload, increasing the stroke volume and therefore increasing cardiac output. 

Afterload also affects the stroke volume in that an increase in afterload will decrease stroke volume. 

Heart rate is affected by the chronotropy, dromotropy, and lusitropy of the myocardium. 

Systemic vascular resistance is determined primarily by the radius of the blood vessels. 

Decreasing the radius of the vessels increases vascular resistance. 

Increasing the radius of the vessels would have the opposite effect. 

Blood viscosity can also affect systemic vascular resistance. 

An increase in hematocrit will increase blood viscosity and increase systemic vascular resistance. 

Viscosity, however, is considered only to play a minor role in systemic vascular resistance.

Common formula:

MAP = Diastolic blood pressure + 1/3 (Systolic Blood pressure – Diastolic Blood Pressure)

          = DBP + 1/3(SBP – DBP) or 

MAP = DBP + 1/3(Pulse Pressure)

MAP = [Systolic Blood Pressure + (2 x Diastolic Blood Pressure)]

                                                      3

Example, if blood pressure is 82 mm Hg/50 mm Hg,

MAP = SBP + 2 (DBP) = 82 +2 (50) = 182 = 60.67 mmHg; or

                3                              3              3

MAP = 1/3 (SBP – DBP) + DBP = 1/3 (82-50) + 50 = 10.67 + 50 = 60.67 mmHg

In sepsis, vasopressors are often titrated based on the MAP. 

In the guidelines of the Surviving Sepsis Campaign, it is recommended that MAP be maintained ≥ 65 mm Hg.

Chronotropy = Heart Rate

Dromotropy = Speed of electrical conduction in the Heart

Lusitropy = Rate of myocardial relaxation

Inotropy = Contractility

Mean Arterial Pressure (MAP) = 70-100 mmHg

Cardiac Index (CI) = Cardiac Output (CO)/ Body Surface Area (BSA) 

                               = 2.5-4 L/min/m2.

Stroke volume (SV) = Cardiac output / Heart Rate 

                                 = 60-120 mL/beat.

Systemic vascular resistance (SVR) = (MAP – Mean Right Atrial Pressure) x 80 / CO 

                                                          = 800-1200 dynes x sec/cm3.

Pulmonary Vascular Resistance = (Mean Pulmonary Artery Pressure – Mean Pulmonary Capillary Wedge Pressure) X 80 / Cardiac Output 

                                                 =125-250 dynes X sec/cm3.

Pulse Pressure (PP)

Pulse Pressure (PP) = Systolic Blood Pressure – Diastolic Blood Pressure

Normal pulse pressure, approximately 40 mmHg.

Change in pulse pressure (Delta Pp) = Volume change (Delta-V) = Stroke volume (SV)

                                                                 Arterial compliance (C)     Arterial compliance (C)

                                                                         

                                                            = Approximately 80 mL = Approximately 40 mm Hg

                                                                       2 mL/mm Hg

Arterial compliance (C) = Delta V/Delta P

Because the aorta is the most compliant portion of the human arterial system, the pulse pressure is the lowest. Compliance progressively decreases until it reaches a minimum in the femoral and saphenous arteries, and then it begins to increase again. 

Narrowed PP (Low) < 25% of the SBP.

Widened PP (High) > 100 % of SBP.

Widened (High) Pulse Pressure (PP)

> 100 % of SBP

Indicative of a noncompliant stiff aorta with a reduced ability to distend and recoil.

With age there is a decrease in compliance of the aorta & small arteries.

In majority, SBP increase while DBP remain near normal. 

In aortic regurgitation (AR), backward, or regurgitant flow, increase SBP and decrease DBP, and therefore increased PP.

Heart valve conditions (Aortic regurgitation, Aortic sclerosis)

Reduced blood viscosity (Severe Iron deficiency anemia)

Increased systolic pressure (Hyperthyroidism), 

Less compliant arteries (Arteriosclerosis)

Narrow (Low) Pulse Pressures (PP)

< 25% of the SBP

Decreased pumping (Heart failure), 

Decreased Stroke Volume (Aortic Stenosis)

Decreased Blood Volume (Blood loss), 

Decreased Filling Time (Cardiac Tamponade/Pericarditis). 

Dysautonomia/postural orthostatic tachycardia syndrome (POTS)

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Rheumatoid Lung Disease

• RA-associated interstitial lung disease (RA-ILD).
• Pleural disease (pleural thickening/effusions).
• Airway disease (Both upper & lower airway).
• Rheumatoid nodules
• Drug-induced lung toxicity (i.e., Methotrexate-induced lung injury)
• Fibro-bullous disease
• Thoracic cage immobility
• Venous thromboembolic disease
• Vasculitis
• Pneumonia.

RHEUMATOID EFFUSION:

• WCC <5000/mm3
• Fluid glucose <60 mg/Dl
• Pleural fluid to serum glucose ratio < 0.5
• pH < 7.3
• High pleural LDH level (ie, > 700 IU/L)
• Cytology: Slender or elongated multinucleated macrophages, round giant multinucleated macrophages, and necrotic background debris.

Pulmonary function testing in ILD (PFT):

• Reduced VC, lung volumes, & DLCO.
• Oxygen desaturation during exercise.
• Restrictive abnormalities common (poor muscle strength or kyphosis due to osteoporosis rather than ILD).

 

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Albuminuria

• Indicator of kidney damage and / or a biomarker of systemic diseases dates back to 1969, when elevated albumin levels were first demonstrated in the urine of patients with newly diagnosed diabetes.

• Urine dipstick is a relatively insensitive marker for albuminuria, not becoming positive until albumin excretion exceeds 300-500 mg/day. 
• Normal rate of albumin excretion is < 30 mg/day (20 mcg/min).
• Persistent albumin excretion between 30-300 mg/day (20 to 200 mcg/min) is called moderately increased albuminuria (formerly called "microalbuminuria").
• Excretion > 300 mg/day (200 mcg/min) represents overt or dipstick positive proteinuria (severely increased albuminuria [formerly called "macroalbuminuria"].

• Albuminuria reflects functional and / or structural changes in the glomerular filtration membrane that allow increased leakage of albumin into primary urine in amounts exceeding the reabsorption capacity of the proximal nephron tubules. 
• Albuminuria considered as an indicator of early damage (dysfunction) of the vascular endothelium (including the glomerular vessels), which leads to increased permeability of the vascular wall. 

• Relationship between albuminuria and cardiovascular risk has been shown in studies of the general population. 
• It is linear and risk is independent of eGFR. 
• Associated with arterial stiffness assessed by the pulse wave velocity measurement

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Lactate Dehydrogenase.

• Cytoplasmic enzymes present in tissues throughout the body.
• Oxidoreductase, enzyme of the anaerobic metabolic pathway.
• Heart, muscle, kidney, lung, and RBC’s have the highest concentration.
• Upon tissue damage, the cells release LDH in the bloodstream.
• Drugs that can increase LDH include alcohol, aspirin, fluorides, narcotics, anesthetics, clofibrate, mithramycin, and procainamide.
• Cancer cells employ LDH to increase their aerobic metabolism (glycolysis, ATP production, & lactate production): Warburg effect.
• CSF LDH increases in bacterial meningitis (normal in viral meningitis).
• Cancer cells undergo LDH mediated energy production to fulfill the demand for fast cellular growth (marker of metastases, prognosis, survival rates., and radiosensitivity).
• LDH serves as a general indicator of acute and chronic diseases.
• LDH helps in distinguishing exudate from transudate effusions.
• Isozymes, named LDH-1 through LDH-5, have differential expression in different tissues.

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Bile acids

 

Role of Bile acids

• Bile acids play a key role in the absorption of lipids in the small intestine. 
• Contribute to cholesterol metabolism by promoting the excretion of cholesterol. 
• Denature dietary proteins, thereby accelerating their breakdown by pancreatic proteases. 
• Direct and indirect antimicrobial effects. In this capacity, recent evidence suggests bile acids are mediators of high-fat diet-induced changes in the gut microbiota. 
• Act as signaling molecules outside of the gastrointestinal tract.

The primary bile acids—cholic acid and cheno-deoxycholic acid—are synthesized from cholesterol in the liver.

The maximal rate of bile acid synthesis is on the order of 4 to 6 g/day.

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