Niacin Deficiency

Distinctive dark red rash appears on the hands, feet, calves, neck, and face, and the tongue and mouth turn dark red.

Many people with niacin deficiency also have deficiencies of protein, riboflavin (a B vitamin), and vitamin B6.

Pellagra develops only if diet is deficient in niacin & tryptophan (body can convert tryptophan to niacin).

Affects the skin, digestive tract, & brain.

Also develops in:

Hartnup disease (absorption of tryptophan is impaired), & Carcinoid syndrome (tryptophan is not converted to niacin).

Alcoholism & isoniazid can lead to a deficiency of niacin.

The diagnosis of niacin deficiency is based on the diet history and symptoms. Measuring a by-product of niacin in urine can help establish the diagnosis, but this test is not always available. The diagnosis is confirmed if niacin relieves symptoms.

Treatment: Nicotinamide, unlike nicotinic acid, does not cause flushing, itching, burning, or tingling sensations.

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White Blood Cell Scan

 

Indium 111- tagged white blood cell scan is a type of imaging modality used to help identify regions of inflammation and thus infections when other imaging studies are equivocal or contraindicated.

The test is used for diagnostic purposes in the evaluation of prosthetic joint infections, osteomyelitis, vascular graft infections, intra-abdominal infections, abscesses, endocarditis, foot ulcers, infected implanted devices such as central venous catheters, fevers of unknown origin when there is a high probability of infection, and Inflammatory bowel disease.

Sensitivity 60 to 100% and specificity 69 to 92%.

White blood cells are obtained from a blood sample from a patient, are tagged with the radioisotope indium-111, and then re-injected intravenously into the patient. These labeled leukocytes localize to a region of inflammation visible on the whole body or regional nuclear imaging with bone scintigraphy.

Recommended dose for adults is 0.3 to 0.5 mCi

Prior IV antibiotics may produce false negative result.

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Pneumobilia vs Portal venous gas

 

Pneumobilia

Also known as aerobilia. Accumulation of gas in the biliary tree. Seen as linear branching gas within liver most prominent in central large caliber ducts as the flow of bile pushes gas toward the hilum. Gas within the biliary tree tends to be more central, whereas gas within the portal venous system tends to be peripheral (carried along by the blood). Also, biliary gas is anti-dependent, and typically fills the left lobe of the liver.

“Saber sign”: Supine radiographs often demonstrate a sword-shaped lucency in the right paraspinal region representing gas from the common duct and the left hepatic duct. Present in ~50% of patients with pneumobilia.

Portal venous gas

Peripheral small caliber branching gas (lucencies) projected in the liver or vessels coursing towards the Liver (away from the hilum).

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High output Ileostomies

 

• Output >1.5 -2.0 L/24 hours leading dehydration & dys-electrolytemia.
• Occurs in 31% of small bowel stomas.
• Daily output increases with increasing small bowel resection
• Resection of 15-50cm of terminal ileum results in an increase of >300 g/24hr vs with <15cm removed 
• Mature ileostomy put out up to 1200mL/day
• Jejunostomies can put out up to 6 L/day
• Colostomies usually only put out 200-600mL/day 
  
  
  

Normal intestinal fluid transport

• 9 -10 L of fluid passes the ligament of Treitz/ day
• Jejunum absorbs ~ 6 L & Ileum ~ 2.5 L
• Colon absorbs rest but 100 mL excreted in feces daily.

Ostomy at ileocecal valve expected to produce 1-1.5 L of stool output/day

Containing approximately

• 200 mEq of sodium
• 100 mEq of chloride &
• 10 mEq of potassium
  
  
  

In Extensive ileal resection, >100 cm, bile salts loss outpaces hepatic production, leading to bile acid deficiency & steatorrhea

Hypomagnesemia occurs in 78% with a jejunostomy.

Common complications include:

• - Dehydration & AKI
• - Low serum sodium
• - Low urinary sodium
• - Low serum magnesium
• - Loss of Chloride & bicarbonate leading to metabolic acidosis
• - High plasma renin & aldosterone
• - Weight loss / malnutrition
• - Low Vitamin B12 (if > 60-100cm of terminal ileum resected)
  
  
  

Management:

Rehydrate & replace electrolytes

Oral hypotonic fluid is restricted & a glucose-saline solution is sipped.

Medication

• To slow transit (Imodium/Lomotil/opioids) or
• To reduce secretions (omeprazole for gastric acid)
• Octreotide/sandostatin
  
  
  
• GLP-2, enhances gut adaptation, inhibits gastric acid secretion & slow emptying; stimulates intestinal blood flow; increases intestinal barrier function; & enhances nutrient & fluid absorption. 

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Sudden Cardiac Death

 Sudden Cardiac Death

Occurs within one hour of the onset of symptoms.

CAD (most common 80%)

(Icy Idiots Chased Hot Vain Chimps)

1. Ischemic Heart disease (MI)
2. Inherited Channelopathies (QT syndrome)
3. Cardiomyopathies (OH, HCM, Myocarditis)
4. Heart Failure (EF less than 35%)
5. Valve disease (Aortic stenosis)
6. Congenital disease (Tetraology of Fallot)

The proximal cause of SCD in most instances is either ventricular fibrillation (VF) or ventricular tachycardia (VT). However, in a significant minority of cases, asystole or pulseless electrical activity is the initial documented rhythm.

The step to improving outcomes involves the chain of survival:

1. Immediate recognition of cardiac arrest and activation of the emergency response system.
2. Early CPR with an emphasis on chest compressions.
3. Rapid defibrillation.
4. Effective advanced life support; and
5. Integrated post-cardiac arrest care.

References:

1. https://www.ncbi.nlm.nih.gov/books/NBK507854/#:~:text=Sudden%20cardiac%20death%20(SCD)%20is,to%20maintain%20perfusion%20and%20life.
2. https://www.ahajournals.org/doi/full/10.1161/01.cir.98.21.2334

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Beta-Blocker Overdose/toxicity

• Bradycardia & hypotension (most common). 
• Myocardial depression & cardiogenic shock (severe overdoses). 
• Ventricular dysrhythmias (Common with propranolol & acebutolol). 
• Others (mental status change, seizure, hypoglycemia, & bronchospasm). 
• Co-ingestions of CCB, TCA, & neuroleptics, increases mortality. 
• Mostly symptomatic < 2 hrs following ingestion, & nearly all develop symptoms < 6 hrs. 
• Delayed toxicity up to 24 hrs after ingestion (Sustained release meds: metoprolol succinate & sotalol). 
• Sotalol prolongs the QTc interval & can lead to Torsades de Pointes. 
• Carvedilol (associated with edema & toxic epidermal necrolysis). 
• IV lipid emulsion therapy for poisoning involving lipophilic medications (eg, propranolol, metoprolol, labetalol).

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QT/QTc- Interval

• Start of Q-wave to end of the T-wave (time of ventricular depolarization + repolarization). 
• Life threatening risk of prolonged QTc >500ms = Torsades de pointes (TdP).
• Prolonged QT/QTc interval may be a clue to electrolyte disturbances (hypocalcemia or hypokalemia), drug effects (quinidine, procainamide, amiodarone, or sotalol), or myocardial ischemia (usually with prominent T wave inversions). 
• Shortened QT intervals are seen with hypercalcemia and digitalis effect. 
• Each 10-millisecond increase in QTc contributes approx a 5% to 7% additional increase in risk for TdP.
• QTc of 540 milliseconds has a 63% to 97% higher risk of developing TdP than a patient with QTc of 440 milliseconds.

How do you measure it:

• Find a lead with the tallest T wave and count the little boxes from the start of the QRS complex to the point where the T wave comes back down to the isoelectric line. 
• Multiply the number of little boxes by 0.04 seconds. 
• Example if you counted 8 boxes then QT interval is 8 x 0.04 = 0.32 seconds (320 milliseconds).
• QT interval should be less than half the preceding R-R interval (Works for regular rates between 65-90).

Methods of calculating the QTc:

• Bazett formula, QTc = QT / √RR.  
• Fridericia formula (QTc = QT / RR1/3)
• Hodges [QTc = QT + 0.00175 x (HR - 60)]
• Framingham linear regression analysis {QTc = QT + 0.154 x (1 - RR)}
• Karjalainen et al. [QT nomogram] 
• Rautaharju formula, QTc = QT x (120 + HR) / 180

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Rhabdomyolysis

• Rhabdomyolysis is a clinical syndrome that comprises destruction of skeletal muscle with outflow of intracellular muscle content into the bloodstream. 
• The systemic complications associated with rhabdomyolysis result from the leakage of muscle intracellular components into the bloodstream. 
• Elevated Creatine kinase (CK) hallmark of rhabdomyolysis. 
• Defined based on CK values five times above the upper limit of normal. 
• Half-life of CK is 1.5 days; elevated<12hrs, peaks in 3 days, & normalizes in 5 days. 
• Myoglobin half-life of 2-3 hrs & rapidly excreted by kidneys. 
• Rapid & unpredictable metabolism makes myoglobin less useful marker of muscle injury.
• Antibiotics associated with rhabdomyolysis: Daptomycin, macrolides, trimethoprim-sulfamethoxazole, linezolid, fluoroquinolones, and cefdinir. 
• Rhabdomyolysis is associated with hyperkalemia, hypocalcemia, hyperuricemia, and hyperphosphatemia.

Management includes appropriate hydration to improve end-organ perfusion, close monitoring of urine output, correction of electrolyte abnormalities, identification of complications like compartment syndrome, and disseminated intravascular coagulation.

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Evaluation of Leukocytosis:

Evaluation of Leukocytosis: The term 'leukocyte' applies to any cells within the myeloblast, monoblast, & lymphoid lineages. Include granulocytes (neutrophils, eosinophils, & basophils), monocytes, & lymphocytes (B cells, T cells, and natural killer cells). In adults, leukocytosis often defined as white blood cell (WBC) count > 11 × 109/L.

Mature WBC:

• 80-90% remain in storage in bone marrow.
• 2% to 3% circulate freely in peripheral blood;
• The rest stay deposited along the margins of blood vessel walls or in the spleen
• Life span: 2- 16 days (depending on cell type in the peripheral circulation).

LEUCOCYTOSIS WBC > 11,000 per mm3 [11.0 × 109 per L] Reactive: Typically, 11,000 to 30,000 per mm3. Leukemoid reaction: approx. 50,000-100,000 per (e.g., C difficile infection, sepsis, organ rejection, or solid tumors. Leukemias or myeloproliferative disorders: > 100,000 per mm3. Paradoxical neutropenia: typhoid fever, rickettsia infections, brucellosis, & dengue.

Neutrophil bands

• Immature neutrophils
• Morphologically: absence of complete separation of nuclear lobes with a visible distinction between chromatin & parachromatin in the narrowest segment of the nucleus often flagged on 5-part automated differential & confirmed by PBS.

Leukemoid Reaction:  Transient increase in WBC count defined as significant neutrophilia >50x10^9/L in the absence of a myeloproliferative neoplasm. Mature neutrophils seen in a leukemoid reaction. Etiology: sepsis, organ rejection, solid tumors, and bacterial infections. D/D leukemia: increases in blast cells (precursor cells to leukocytes) and immature WBCs, Improves after treating the underlying cause.

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Hyponatremia

Hyponatremia (<135 mEq/L) is a common electrolyte abnormality caused by an excess of total body water in comparison to that of the total body sodium content. Measuring the serum osmolality, urine sodium concentration and urine osmolality helps to differentiate among the possible causes. The severity of this electrolyte abnormality ranges from asymptomatic to seizures, coma and death as a consequence of cerebral swelling.

Pseudohyponatremia is due to hypertriglyceridemia or multiple myeloma. In regular subjects, the plasma water is 93% of the plasma volume. Plasma water part falls lower than 80% in cases with noticeable hyperlipidemia (triglycerides >1500 mg/dL) or hyperproteinemia (protein >10 mg/dL). Rise in blood urea causes the hyponatremia in renal failure.

True hyponatremia is having a fall in serum osmolality and is divided into hypervolemic, hypovolemic, and euvolemic based on volume status. 

Osmoreceptors in the hypothalamus detect the plasma osmolality. If Posm >285 mOsm/kg, osmoreceptors stimulate the release of anti-diuretic hormone (ADH) from the posterior pituitary into the circulation, as well as stimulate thirst. ADH release is also stimulated in states of low effective circulating volume. Circulating ADH binds to receptors on the principal cells of the collecting duct in the kidneys and activates a cellular pathway which ultimately results in water reabsorption. This results in a decrease in the serum osmolality and an increase in the urine osmolality (Uosm).  In certain states, ADH can be released inappropriately or ectopically, meaning that ADH is released without an osmotic or hemodynamic stimulus. When ADH is suppressed, water is renally excreted. 

Another important physiological pathway is the renin-angiotensin-aldosterone system (RAAS). This pathway is activated in states of low effective circulating volume and/or when there is reduced sodium in the renal tubules. These conditions stimulate the release of renin from the juxtaglomerular cells, which are part of the afferent arterioles. The activation of RAAS ultimately results in increased sodium reabsorption, arteriolar vasoconstriction and release of ADH from the posterior pituitary. Measured urine sodium concentration (UNa) is a reflection of intravascular volume; UNa is elevated with volume expansion and reduced with volume depletion. 

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Para-neoplastic dermatoses (PD)

Para-neoplastic dermatoses (PD):

• Heterogeneous, rare, acquired diseases characterized by the presence of an underlying neoplasia.
• Usually develop simultaneously with the underlying cancer, but they can also occur before or after the development of the neoplasia.
• Their recognition can lead to a prompt cancer detection and to an early start of the appropriate therapy.

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Diabetic Ketoacidosis (DKA)

Diagnostic Criteria:

• Serum glucose >250 mg/dL
• Arterial pH <7.3
• Serum bicarbonate <18 mEq/L
• At least moderate ketonuria or ketonemia.

10% to 30% of DKA cases occur in patients with type 2 diabetes, in situations of extreme physiologic stress or acute illness.

Infection is a very common trigger for DKA in patients who have new-onset diabetes and previously established diabetes. If there is any suspicion of infection, antibiotics should be administered promptly.

2.6% to 3.2% of DKA admissions are Euglycemic Diabetic ketoacidosis (EDKA).

Pregnancy is a risk factor for EDKA because of the physiologic state of hypoinsulinemia and increased starvation.
Alcoholic ketoacidosis may have a similar presentation to EDKA, with anorexia, vomiting, dyspnea, and significant anion gap metabolic acidosis and ketonemia.

Common, early signs of ketoacidosis include nausea, vomiting, abdominal pain, and hyperventilation.

Patients with DKA usually present with a serum anion gap greater than 20 mEq/L (normal 3 to 10 mEq/L). However, the increase in anion gap is variable, being determined by several factors: the rate and duration of ketoacid production, the rate of metabolism of the ketoacids and their loss in the urine, and the volume of distribution of the ketoacid anions.

Continue insulin infusion until ketoacidosis is resolved, serum glucose is below 200 mg/dL, and subcutaneous insulin is begun. Treatment with IV fluid resuscitation should continue until the anion gap closes and acidosis has resolved.

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