Asymptomatic microscopic hematuria

 The prevalence of asymptomatic microscopic hematuria in adults ranges from 0.19 to 21 percent. Patients with asymptomatic microscopic hematuria or with hematuria persisting after treatment of urinary tract infection also need to be evaluated. Because upper and lower urinary tract pathologies often coexist, patients should be evaluated using cytology plus intravenous urography, computed tomography, or ultrasonography. When urine cytology results are abnormal, cystoscopy should be performed to complete the investigation.

Microscopic hematuria generally is defined as one to 10 red blood cells per high-power field of urine sediment. The American Urological Association (AUA) defines clinically significant microscopic hematuria as three or more red blood cells per high-power field on microscopic evaluation of urinary sediment from two of three properly collected urinalysis specimens. May be associated with urologic malignancy in up to 10 percent of adults.

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Antiarrhythmic Medications

 Antiarrhythmic Medications - Vaughan-Williams Classification

 • Class I (Ia, Ib, Ic)

 • Class II

 • Class III

 • Class IV

 • Other anti-antiarrhythmic drugs: Adenosine, Digoxin, Ivabradine

Satyendra Dhar, MD 

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D-dimer & interpretation

D-dimer is the smallest fibrinolysis-specific degradation product found in the circulation. The D-dimer is very sensitive to intravascular thrombus and may be markedly elevated in disseminated intravascular coagulation, acute aortic dissection, and pulmonary embolus. Because of its exquisite sensitivity, negative tests are useful in the exclusion venous thromboembolism. Elevations occur in normal pregnancy, rising two- to fourfold by delivery. D-dimer also rises with age, limiting its use in those > 80 years old. There is a variable rise in D-dimer in active malignancy and indicates increased thrombosis risk in active disease. Elevated D-dimer following anticoagulation for a thrombotic event indicates increased risk of recurrent thrombosis. 

Satyendra Dhar MD

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Lactic acid & interpretation

 

Lactic acid was first found & described in sour milk by Karl Wilhelm Scheele in 1780. German physician–chemist Johann Joseph Scherer (1841–1869) demonstrated the occurrence of lactic acid in human blood under pathological conditions in 1843 & 1851.

Lactic acid is essentially a carbohydrate within cellular metabolism and its levels rise with increased metabolism during exercise and with catecholamine stimulation. Glucose-6-phosphate is converted anaerobically to pyruvate via the Embden-Meyerhof pathway. Pyruvate is in equilibrium with lactate with a ratio of about 25 lactate to 1 pyruvate molecules. Thus, lactate is the normal endpoint of the anaerobic breakdown of glucose in the tissues.

The causes of lactic acidosis can generally be divided into those associated with obviously impaired tissue oxygenation (type A) and those in which systemic impairment in oxygenation does not exist or is not readily apparent (type B). However, there is frequently overlap between type A and type B lactic acidosis. In sepsis, for example, there is both an increase in lactate production resulting from microcirculatory failure and also a decrease in lactate clearance that is not solely due to diminished oxygen delivery.

Satyendra Dhar MD, 

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Monkeypox

 Monkeypox is a viral zoonotic infection that results in a rash similar to smallpox. However, person-to-person spread outside the household and mortality from a monkeypox infection are significantly less than for smallpox. The rash of monkeypox can also be similar in appearance to more common infectious rashes, such as those observed in secondary syphilis, herpes simplex infection, and varicella-zoster virus infection.

WHO has activated its highest alert level for the growing monkeypox outbreak, declaring the virus a public health emergency of international concern.

Monkeypox is a rare disease caused by infection with the monkeypox virus. Monkeypox virus is part of the same family of viruses as variola virus, the virus that causes smallpox. Monkeypox symptoms are similar to smallpox symptoms, but milder, and monkeypox is rarely fatal. Monkeypox is not related to chickenpox.

Symptoms of monkeypox can include:

• ·         Fever
• ·         Headache
• ·         Muscle aches and backache
• ·         Swollen lymph nodes
• ·         Chills
• ·         Exhaustion
• ·         Respiratory symptoms (e.g. sore throat, nasal congestion, or cough)
• ·         A rash that may be located on or near the genitals (penis, testicles, labia, and vagina) or anus (butthole) but could also be on other areas like the hands, feet, chest, face, or mouth.

o   The rash will go through several stages, including scabs, before healing.

o   The rash can look like pimples or blisters and may be painful or itchy.

Source : CDC/WHO

Satyendra Dhar MD

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Candida glabrata

 Candida glabrata was considered a relatively nonpathogenic commensal fungal organism of human mucosal tissues. However, with the increased use of immunosuppressive agents, mucosal and systemic infections caused by C. glabrata have increased significantly, especially in the human immunodeficiency virus-infected population. A major obstacle in C. glabrata infections is their innate resistance to azole antimycotic therapy, which is very effective in treating infections caused by other Candida species. Candida glabrata, formerly known as Torulopsis glabrata, contrasts with other Candida species in its nondimorphic blastoconidial morphology and haploid genome. C. glabrata currently ranks second or third as the causative agent of superficial (oral, esophageal, vaginal, or urinary) or systemic candidal infections, which are often nosocomial.

Satyendra Dhar MD,

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Acute limb ischemia (ALI) & Critical Limb ischemia (CLI)

Acute limb ischemia (ALI)

Rapid decrease in lower limb blood flow due to acute occlusion of a peripheral artery or bypass graft and etiology are broadly divided into embolism and thrombosis with various comorbidities. The symptoms of ALI are abrupt with pain, numbness, and coldness of the lower limb, and paresthesia, contracture, and irreversible purpura will appear with the exacerbation of ischemia.

Critical Limb ischemia

Etiology: obstructive atherosclerotic disease; atheroembolic or thromboembolic disease, vasculitis, in situ thrombosis related to hypercoagulable states, thromboangiitis obliterans, cystic adventitial disease, popliteal entrapment, or trauma.

pathophysiology: chronic & complex process that affects the macrovascular, microvascular systems & surrounding tissues.

The twin Saints Comas and Damian were ascribed to have saved a gangrenous limb in the 13th century and became patrons of future surgeons. In the 1960s, Charles Dotter developed techniques to image diseased arteries during a recanalization procedure. The development of guide wires, angioplasty balloons, & stents quickly followed.

Satyendra Dhar MD, 

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HYPOMAGNESEMIA

 HYPOMAGNESEMIA

If unsure, the distinction between gastrointestinal losses and renal losses can be made by measuring the 24-hour urinary magnesium excretion. In addition, one can calculate the fractional excretion of magnesium (on a random urine specimen) with the following formula where U and P refer to the urine and plasma concentrations of magnesium (Mg) and creatinine (Cr).

FEMg  = [(UMg x PCr) / (PMg x UCr x 0.7)] x 100

If the fractional excretion of magnesium is above 2% in someone with normal renal function, the hypomagnesemia is likely secondary to renal magnesium wasting from drugs such as diuretics, aminoglycosides, or cisplatin.

2 grams of IV magnesium sulfate increased serum levels by a paltry median of 0.2 mg/dL.  

Rechecking too soon may give a false sense of security.

• If the Magnesium level is 1.7 to 2, give 2 grams of MgSO4 IV.
• If the Magnesium level is 1.3 to 1.7 give 4 grams of MgSO4  IV.

Parenteral (IV or IM): Magnesium Sulfate (MgSO4)

Magnesium Sulfate is 10% elemental (1 gram of Magnesium per 100 ml solution)

• One gram of MgSO4 contains 8.12 meq of Magnesium
• One ml MgSO4 50% Solution = 4 meq Magnesium
• One ml MgSO4 10% Solution = 0.8 meq Magnesium

Satyendra Dhar MD, 

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INSULIN CONVERSION

 INSULIN CONVERSION

A total daily dose of insulin (TDD) =

             N X Wt in Kg

(N= 0.5-1.0 for obese, resistant & most type 2 DM)

Administer:

 ½ as Basal (Long acting) & ½ in 3 divided doses a day before each meal

Target pre-meal BG < 140 & random BG < 180 in non-ICU pts

For patients who aren’t transitioning from IV insulin or who aren’t on an insulin regimen at home, many experts offer these rules of thumb for estimating the total daily dose:

* 0.3 units/kg/day for patients who are lean, on hemodialysis, frail and elderly, insulin-sensitive, or at risk for hypoglycemia;

* 0.4 units/kg/day for a patient at normal weight;

* 0.5 units/kg/day for overweight patients; and

* 0.6 units/kg/day or more for patients who are obese, on high-dose steroids, or insulin-resistant.

Satyendra Dhar MD, 

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UROLITHIASIS

 UROLITHIASIS

80% of stones are composed of calcium oxalate or phosphate. Others include uric acid (9%), struvite (10%), & cystine (1%) stones. Struvite stones can form into a staghorn or large calculus that overwhelms the renal collecting system; are Mg ammonium phosphate; secondary to elevated urine pH, & urease forming Proteus or Klebsiella species.

Urea breakdown yields ammonia as a by-product, which increases the urinary pH (typically to more than 8), and facilitates struvite stone formation.

Uric acid stone formation is related to low urinary uric acid levels, low urine pH, and low urinary volume. Most commonly, these patients will present as idiopathic uric acid stone formers; however, metabolic disorders such as diabetes and obesity will also increase the risk of uric acid stones.

Cystine stones are rare and occur due to an inborn congenital disorder causing mutations in 2 genes, SLC3A1, and SLC7A9. These mutations cause defective cystine metabolism and transport, resulting in cystinuria and stones.

Satyendra Dhar MD,

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GRADING in clinical medicine

 GRADING in clinical medicine

The grading system is often used in Clinical medicine to indicate the severity scale of a disease or a pathology. Below are some of the grading systems used often in daily practice. Please comment & add if you know of any other grading systems.

Satyendra Dhar MD,

 

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ACUTE COMPARTMENT SYNDROME

 ACUTE COMPARTMENT SYNDROME

The definitive surgical therapy for compartment syndrome is emergent fasciotomy (compartment release), with subsequent fracture reduction or stabilization and vascular repair, if needed. The goal of decompression is the restoration of muscle perfusion within 6 hours.

The original description of the consequences of unchecked rising intra-compartmental pressures is widely attributed to Richard von Volkmann.

In acute compartment syndrome, especially with trauma, consider performing a workup for rhabdomyolysis, with measurement of the following:

* Creatine phosphokinase (CPK)

* Renal function studies

* Urinalysis

* Urine myoglobin

Satyendra Dhar MD, 

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