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 Pseudomonas aeruginosa and antibiotics.


Malnutrition is an imbalance between the nutrients your body needs to function and the nutrients it gets. It is an independent risk factor that negatively influences patients’ clinical outcomes, quality of life, body function, and autonomy. Early identification of patients at risk of malnutrition or who are malnourished is crucial in order to start a timely and adequate nutritional support. Nutrition support refers to enteral or parenteral provision of calories, protein, electrolytes, vitamins, minerals, trace elements, and fluids.

Historically, serum proteins such as albumin and prealbumin (i.e. transthyretin) have been widely used by physicians to determine patients’ nutritional status. Other markers that have been studied include retinol-binding protein (RBP), transferrin, total cholesterol and indicators of inflammation such as C-reactive protein (CRP) and total lymphocyte count (TLC).









Calcific aortic valve stenosis is characterized by a progressive fibro-calcific remodeling and thickening of the aortic valve cusps, which subsequently leads to valve obstruction. The underlying pathophysiology is complex and involves endothelial dysfunction, immune cell infiltration, myofibroblastic and osteoblastic differentiation, and, subsequently, calcification.

Among symptomatic patients with medically treated moderate-to-severe aortic stenosis, mortality from the onset of symptoms is approximately 25% at 1 year and 50% at 2 years. Symptoms of aortic stenosis usually develop gradually after an asymptomatic latent period of 10-20 years.

Systolic hypertension can coexist with aortic stenosis. The carotid arterial pulse typically has a delayed and plateaued peak, decreased amplitude, and gradual downslope (pulsus parvus et tardus).

Other symptoms of aortic stenosis include the following:

  • Pulsus alternans: Can occur in the presence of left ventricular systolic dysfunction
  • Hyperdynamic left ventricle: Unusual; suggests concomitant aortic regurgitation or mitral regurgitation
  • Soft or normal S1
  • Diminished or absent A2: The presence of a normal or accentuated A2 speaks against the existence of severe aortic stenosis
  • Paradoxical splitting of the S2: Resulting from late closure of the aortic valve with delayed A2
  • Accentuated P2: In the presence of secondary pulmonary hypertension
  • Ejection click: Common in children and young adults with congenital aortic stenosis and mobile valve leaflets
  • Prominent S4: Resulting from forceful atrial contraction into a hypertrophied left ventricle
  • Systolic murmur: The classic crescendo-decrescendo systolic murmur of aortic stenosis begins shortly after the first heart sound; the intensity increases toward mid systole and then decreases, with the murmur ending just before the second heart sound.


Furosemide is a loop diuretic. 
  • Inhibits the reabsorption of sodium and chloride from the loop of Henle and distal renal tubule.
  • Increases renal excretion of water, sodium, chloride, magnesium, potassium, and calcium.
  • Effectiveness persists in impaired renal function.
Pharmacokinetics
  • Absorption: 60–67% absorbed after oral administration (↓ in acute HF and in renal failure); also absorbed from IM sites; IV administration results in complete availability; 99.6% absorbed after SUBQ administration.
  • Protein Binding: 91–99%.
  • Metabolism and Excretion: Minimally metabolized by liver, some non-hepatic metabolism, some renal excretion as unchanged drug.
  • Half-life: 30–120 min (↑ in renal impairment).


 Peritonitis is defined as an inflammation of the serosal membrane that lines the abdominal cavity and the organs contained therein. Depending on the underlying pathology, the resultant peritonitis may be infectious or sterile (ie, chemical or mechanical).

Peritoneal infections are classified as primary (ie, from hematogenous dissemination, usually in the setting of an immunocompromised state), secondary (ie, related to a pathologic process in a visceral organ, such as perforation or trauma, including iatrogenic trauma), or tertiary (ie, persistent or recurrent infection after adequate initial therapy). Primary peritonitis is most often spontaneous bacterial peritonitis (SBP) seen mostly in with chronic liver disease. Secondary peritonitis is by far the most common form of peritonitis encountered in clinical practice. Tertiary peritonitis often develops in the absence of the original visceral organ pathology.

Infections of the peritoneum are further divided into generalized (peritonitis) and localized (intra-abdominal abscess).


Hypomagnesemia is common among hospitalized patients and frequently occurs with other electrolyte disorders, including hypokalemia and hypocalcemia. Magnesium depletion usually results from inadequate intake plus impairment of renal conservation or gastrointestinal absorption.

Drugs can cause hypomagnesemia. Examples include chronic (> 1 year) use of a proton pump inhibitor and concomitant use of diuretics. Amphotericin B can cause hypomagnesemia, hypokalemia, and acute kidney injury. The risk of each of these is increased with duration of therapy with amphotericin B and concomitant use of another nephrotoxic agent. Liposomal amphotericin B is less likely to cause either kidney injury or hypomagnesemia.

Trousseau sign is the precipitation of carpal spasm by reduction of the blood supply to the hand with a tourniquet or blood pressure cuff inflated to 20 mm Hg above systolic blood pressure applied to the forearm for 3 minutes.

Chvostek sign is an involuntary twitching of the facial muscles elicited by a light tapping of the facial nerve just anterior to the exterior auditory meatus.

Serum magnesium concentration < 1.8 mg/dL

Hypomagnesemia is diagnosed by measurement of serum magnesium concentration.

Severe hypomagnesemia usually results in concentrations of < 1.25 mg/dL.

Associated hypocalcemia and hypocalciuria are common.

Hypokalemia with increased urinary potassium excretion and metabolic alkalosis may be present.

Treatment with magnesium salts is indicated when magnesium deficiency is symptomatic or the magnesium concentration is persistently < 1.25 mg/dL. Patients with alcohol use disorder are treated empirically. In such patients, deficits approaching 12 to 24 mg/kg are possible.

When serum magnesium is ≤ 1.25 mg/dL but symptoms are less severe, magnesium sulfate may be given IV in 5% D/W at a rate of 1 g/hour as slow infusion for up to 10 hours. In less severe cases of hypomagnesemia, gradual repletion may be achieved by administration of smaller parenteral doses over 3 to 5 days until the serum magnesium concentration is normal. 

 

Procalcitonin (PCT) has developed into a promising new biomarker for early detection of (systemic) bacterial infections. PCT is a 116-amino acid residue that was first explained by Le Moullec et al. in 1984; however, its diagnostic significance was not recognized until 1993. In 1993, Assicot et al. demonstrated a positive correlation between high serum levels of PCT and patients with positive findings for bacterial infection and sepsis (eg, positive blood cultures). PCT assays with a specificity of 79%, is utilized to more accurately determine if a bacterial species is the cause of a patient’s systemic inflammatory reaction.

Procalcitonin serum levels have been shown to increase 6 to 12 hours following initial bacterial infections and increase steadily 2 to 4 hours following the onset of sepsis. The half-life of PCT is between 20 to 24 hours; therefore, when a proper host immune response and antibiotic therapy are in place, PCT levels decrease accordingly by 50% over 24 hours.

PCT serum levels can become elevated among patients during times of noninfectious conditions, such as with trauma, burns, carcinomas (medullary C-cell, small cell lung, & bronchial carcinoid), immunomodulator therapy that increase proinflammatory cytokines, cardiogenic shock, first 2 days of a neonate's life, during peritoneal dialysis treatment, and in cirrhotic patients (Child-Pugh Class C). Furthermore, PCT levels have found to be falsely elevated in patients suffering from various degrees of chronic kidney disease which can, in turn, alter baseline results making the determination of an underlying bacterial infection difficult to establish.



 Thoracolumbar Spine Fracture

The most common mechanisms for thoracolumbar traumatic injuries include motor vehicle accidents, falls from height, recreational injuries, and work-related injuries. Most of them are high-velocity and high-energy injuries, which usually involve additional injuries.

The T10-L2 thoracolumbar region is the most common area of injury to the spine from trauma due to the specific biomechanics of this segment of the spine. Injury to this area can result in a permanent neurological deficit from compression or direct injury to the nerve roots of the cauda equina or the conus medullaris and warrants immediate attention and assessment.

American Spinal Injury Association (ASIA) impairment scale:

A - Complete: No motor or sensory function is preserved below the neurological level

B - Incomplete: Sensory function preserved but no motor function is preserved below the neurological level including the S4–S5 segments

C - Incomplete: Motor function is preserved at the most caudal sacral segments for voluntary anal contraction. The motor function below the neurological level is preserved with less than half of key muscles that have a muscle grade ≥ 3

D - Incomplete: Motor function is preserved below the neurological level with at least half of key muscles that have a muscle grade ≥ 3

E - Normal: Motor and sensory function are normal

Compression fracture. While the front (anterior) of the vertebra breaks and loses height, the back (posterior) part of it does not. This type of fracture is usually stable (the bones have not moved out of place) and is rarely associated with neurologic problems. Compression fractures commonly occur in patients with osteoporosis.

Axial burst fracture.  In this type of fracture, the vertebra loses height on both the front and back sides. It is often caused by landing on the feet after falling from a significant height. An axial burst fracture can sometimes result in nerve compression. Some fractures are stable, while others are significantly unstable (the bones have moved out of place).

Hematology Algorithms 

Anemia is described as a reduction in the proportion of the red blood cells. Most patients experience some symptoms related to anemia when the hemoglobin drops below 7.0 g/dL. RBC are produced in the bone marrow and released into circulation. Approximately 1% of RBC are removed from circulation per day. Imbalance in production to removal or destruction of RBC leads to anemia. 

The etiology of anemia depends on whether the anemia is hypo-proliferative (i.e., corrected reticulocyte count <2%) or hyperproliferative (i.e., corrected reticulocyte count >2%).  Hypo-proliferative anemias are further divided by the mean corpuscular volume into microcytic anemia (MCV<80 fl), normocytic anemia (MCV 80-100 fl) & macrocytic anemia (MCV>100 fl). 

Pancytopenia is a hematologic condition characterized by a decrease in all three peripheral blood cell lines. It is characterized by the hemoglobin of less than 12 g/dL in women and 13 g/dL in men, platelets of less than 150,000 per mcL, and leukocytes of less than 4000 per ml (or absolute neutrophil count of less than 1800 per ml). However, these thresholds largely dependent on age, sex, race as well as varying clinical scenarios. 

Leukopenia is primarily seen as neutropenia since neutrophils constitute the majority of the leukocytes. The etiology of pancytopenia can be broadly categorized as a central type that involves production disorders or a peripheral type that involves disorders of increased destruction. These causes could contribute to the pancytopenia independently or as a combination. 

Red cell distribution width (RDW) = (standard deviation of MCV/mean MCV) × 100. 

Normal range11.5–14.5% has suspicion of thalassemia trait & high often indicates IDA 

Mentzer index = (MCV/RBC count). 

< 13 may represent thalassemia trait & >13 often indicates IDA



 Normal coagulation pathway represents a balance between the pro coagulant pathway that is responsible for clot formation and the mechanisms that inhibit the same beyond the injury site. Imbalance of the coagulation system may occur in the perioperative period or during critical illness, which may be secondary to numerous factors leading to a tendency of either thrombosis or bleeding.

The plasma coagulation system in mammalian blood consists of a cascade of enzyme activation events in which serine proteases activate the proteins (proenzymes and procofactors) in the next step of the cascade via limited proteolysis. The ultimate outcome is the polymerization of fibrin and the activation of platelets, leading to a blood clot. This process is protective, as it prevents excessive blood loss following injury (normal hemostasis). Unfortunately, the blood clotting system can also lead to unwanted blood clots inside blood vessels (pathologic thrombosis), which is a leading cause of disability and death in the developed world. There are two main mechanisms for triggering the blood clotting, termed the tissue factor pathway and the contact pathway. Only one of these pathways (the tissue factor pathway) functions in normal hemostasis. Both pathways, however, contribute to thrombosis. 

The blood coagulation cascade culminates with the conversion of fibrinogen to fibrin, essentially transmitting the proteolytic injury signal into a fibrin clot capable of occluding the inciting tissue defect. Fibrinogen is the most abundant coagulation protein in plasma, consistent with its mechanical rather than signaling role.


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