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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Lithium Toxicity

 The mechanism of action of lithium is not known. It is rapidly absorbed, has a small volume of distribution, and is excreted in the urine unchanged (there is no metabolism of lithium).

Toxic levels > 2 mEq/L

Satyendra Dhar MD,

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Statins & Recommendations

Statins & Recommendations:

Word Cholesterol came from Cholesterine, named by French chemist Michel E. Chevreul (‘solid bile’ in Greek: ‘chole’ for bile and ‘stereos’ for solid). The exact formula of cholesterol was established in 1888 by Friedrich Reinitzer. Merck Labs found the first statin, in 1978, in a fermentation broth of Aspergillus terreus, named mevinolin & later lovastatin.

Statins inhibit the critical step of cholesterol synthesis in which 3-hydroxy-3-methylglutaryl coenzyme A (HMGC) is transformed to mevalonate by the enzyme HMGC reductase. By doing so, they have a potent lipid-lowering effect that reduces cardiovascular risk and decreases mortality. Since the mevalonate pathway also influences endothelial function, the inflammatory response, and coagulation, the effects of statins reach well beyond their cholesterol-lowering properties. As with all drugs, statins may have adverse effects; these include musculoskeletal symptoms, increased risk of diabetes, and higher rates of hemorrhagic stroke. However, the frequency of adverse effects is extremely low and, in selected patient populations, the benefits of statins considerably outweigh the potential risks.

Satyendra Dhar MD, 

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SKIN RASHES

 SKIN RASHES

Skin rashes can occur from a variety of factors, including infections, heat, allergens, immune system disorders, and medications.

A rapid and accurate diagnosis is critically important to make treatment decisions, especially when mortality or significant morbidity can occur without prompt intervention.

Rashes can be divided into petechial/purpuric, erythematous, maculopapular, and vesiculobullous. After this differentiation, the presence of fever and systemic signs of illness should be assessed. Through the breakdown of rashes into these classes, emergency providers can ensure deadly conditions are considered.

Satyendra Dhar MD, 

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Nail Findings & Associated Conditions

 Nail Findings & Associated Conditions

Change in color, texture, or shape can be harmless, but may suggest an underlying systemic disease.

 • Muehrcke's Lines

 • Melanoma

 • Terry's Lines

 • Onychogryphosis

 • Clubbed Fingernails

 • Mees' lines

 • Koilonychia

 • Pterygium Unguis

 • Green Nail Syndrome

 • Leukonychia

 • Beau's Lines

 • Yellow Nail Syndrome

 • Onycholysis

 • Transverse Ridging

 • Nail Plate Crumbling

 • Nail Pitting

 • Central Nail Canal

 • Periungual Telangiectasia

 Satyendra Dhar, MD 

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LUDWIG’S ANGINA

 LUDWIG’S ANGINA

This condition was named after a German physician, Wilhelm Friedrich von Ludwig, who first described it in 1836.

Although traditionally associated with pain of cardiac origin, the term “angina” is derived from the Latin word for choke (angere) and the Greek word for strangle (ankhone). In the case of Ludwig’s angina, it refers to the feeling of strangling and choking secondary to lingual airway obstruction, which is the most serious potential complication of this condition.

Ludwig angina is a bilateral infection of the submandibular space that consists of two compartments in the floor of the mouth, the sublingual space, and the submylohyoid (also known as submaxillary) space.

Ludwig's angina usually originates from dental infections in the mandibular molars, particularly the second and third molars, accounting for over 90% of cases.

Satyendra Dhar MD, 

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