Learning Critical Care Medicine

"It does not matter how slowly you go, as long as you do not stop"                                             - Confucious Since the introduction of central venous catheterization by Forssman in 1929, this invasive procedure evolved to be very helpful in management of both inpatient and outpatients. Central venous catheters are used for indication as varied as hemodynamic monitoring, vasopressors administration, renal replacement therapy, administration of chemotherapeutic agents and total parenteral nutrition. But central venous catheters have also evolved to be an important source of healthcare related infection, translating to increased morbidity, mortality and financial burden. Intravenous catheter related blood stream infection is the third leading cause of device related infection, after catheter associated urinary tract infection (CAUTI) and ventilator associated pneumonia (VAP). Intravascular catheter related blood stream infection is one of the ‘ne

"There is only one corner of universe, you can be certain of improving, and that is your own self"                                              - Aldous Huxley Guideline for Management of Spontaneous Intracerebral Hemorrhage: ACC/AHA 2015- Salient points: In patient on oral anticoagulation, coagulopathy should be rapidly corrected.  Patients on vitamin K antagonist (warfarin), should be given vitamin K (5-10 mg intravenous) and fresh frozen plasma or prothrombin complex concentrate (PCC). PCC corrects INR more rapidly, requires less volume and associated with fewer complication compared to fresh frozen plasma. Therefore PCC may be preferred.  Although rFVIIa may correct INR, clotting may not be restored in vivo, as it does replace all clotting factors. Therefore it is not recommended for vitamin K antagonist reversal in ICH. For newer oral anticoagulant (NOAC) like debigatron, rivaroxaban and apixaban, activated charcoal can be useful if given within 2 hou

"Variability is the law of life,  And as no two faces are same, s o no two bodies are alike, And no two individuals react alike and behave alike, Under the abnormal  conditions, which we know as disease."                                                                       - William Olser Lactic acidosis is caused by accumulation of lactate and protons in the body. It is often associated with poor clinical outcomes. The impact of lactic acidosis is determined by its severity, duration and the causative pathophysiology.  Sustained hyperlactatemia in hospitalized patients with diverse disorders is associated with a  large increase in mortality, regardless of status  with respect to shock or hypotension.  Hyperlactatemia is not the same as lactic acidosis. Under physiological pH lactic acid is 99 percent dissociated into lactate and [H + ]. As per steward’s strong ion difference (SID) concept, acid base balance is determined by the independent effect of CO 2 , concen

Causes of lactic acidosis: ●Type A lactic acidosis: caused by impaired tissue oxygen delivery, as in- •anaerobic muscle activity- physical exercise, generalises tonic conic convulsions; •impaired tissue perfusion- global (shock- hypovolemic, cardiac ir sepsis) or regional (mesenteric ischaemia); •impaired tissue oxygen delivery or utilization- carbon monoxide poisoning, severe anemia, hypoximia. ●Type B lactic acidosis: not associated with any evidence of impaired oxygen delivery. It may be due to various mechanism- •Type B1: Associated with disease states- diabetes, hematological malignancies, AIDS, chronic alcoholism, thiamine deficiency; Diabetic patients may develop lactic acidosis of various etiology. This type of lactic acidosis is due to decrease activity of pyruvate dehydrogenase. Increased lactate production by neoplastic cells give rise to lactic acidosis in leukemia and lymphoma. In chronic alcoholics lactic acidosis develops because of hepatic dysfunction and redu

"Heard melodies are sweet, those unheard are sweeter"                       - John Keats Pyroglutamic acid (5-oxoproline) is an intermediate metabolite of gamma glutamyl cycle. Gamma glutamyl cycle is responsible for glutathione synthesis and degradation. Glutathione (gamma glutamyl cysteinyl glycine-GSH) is an antioxidant substance, involved in many biological function, including inactivation of free radicals. Glutathione is synthesized by glutamate, glycine and cysteine. Glutamate and cysteine is converted to gamma glutamyl cysteine, by gamma glutamyl cysteine synthetase (GCS), which then reacts with glycine, in the presence of glutathione synthetase, to produce glutathione. Glutathione is degraded by gamma glutamyl transpeptidase (GGT) and gamma glutamyl cyclotransferase to pyroglutamic acid (5-oxoproline). Pyroglutamic acid (5-oxoproline) is catalyzed by 5-oxoprolinase to glutamate, which enters into gamma glutamyl cycle. Glutathione synthesis is kept

  "Life is struggle, not against sin,    not against money or power,    but against hydrogen ion"                              - H.L. Mencken D lactic acid is a stereo-isomer of L lactic acid. L lactic acid is the principle isomer produced by human and is responsible for usual lactic acidosis. D lactate is produced in small amount in humans, by colonic bacteria, as metabolic product of carbohydrate. D lactic acid is not metabolized by lactate dehydrogenase (which converts L lactate to pyruvate), therefore D lactate is slowly eliminated from body in urine and faeces.  D lactate accumulates in three clinical settings- 1. Short bowel syndrome, 2. Propylene glycol toxicity, 3. Diabetes ketoacidosis. In short bowel syndrome, overgrowth of colonic gram positive anaerobes, like lactobacili, produce D lactate. Increased delivery of glucose and other carbohydrates to colon after resection of small bowel, leads to overproduction of D lactate by the colonic micr

"The fact that patient gets well, does not prove that diagnosis was correct"                                                                  - Samuel J. Meltzer SEROTONIN SYNDROME (SS): SS is characterized by hyperthermia, altered mentation, mydriasis, increased muscle tone, hyperreflexia, clonus, diarrhea and autonomic instability, developing 6-12 hours after exposure to serotonin agonist agents. There is prominent diaphoresis and sialorrhea. Clonus is the most specific sign of SS. Drugs associated with SS are: Selective serotonin reuptake inhibitors (SSRI)- fluoxetine, sertraline, citalopram, escitalopram, Serotonin norepinephrine reuptake inhibitors (SNRI)- venlafaxine, duloxetine,     TCA- clomiperamine, imipramine, trazodone, MAO inhibitors- selegiline, procarbazine, linezolid, furazolidone, Opiates- meperidine, tramadol, fentanyl, dextromethorphan, pentazocine, dextropropxyphene,   Antiemetics- ondansetron, granisetron, metocloperamide,  

"The person who takes medicine must recover twice,  once from the disease, and once from the medicine"                                                         - William Osler NEUROLEPTIC MALIGNANT SYNDROME (NMS): NMS is defined as tetrad of hyperthermia, rigidity, mental status changes and autonomic instability, developing after 24 hours (first 2 weeks) of starting, dose escalating or switching to another, dopamine antagonist medications, including neuroleptics (antipsychotics). Mental status changes can present as coma, stupor, mutism or agitation. Muscle rigidity is characterized by lead pipe type and hyporeflexia. Superimposed tremors may give impression of cogwheel phenomenon. There is prominent diaphoresis and sialorrhea. Usually symptomatology develops over 1 to 3 days, with change in mental status followed by rigidity, then hyperthermia and autonomic dysfunction. Reported incidence of NMS, among patients taking neuroleptic (antipsychotic) medic

"Somewhere something incredible is waiting to be known"                                    - Carl Sagan HEAT STROKE  is caused when thermoregulatory mechanism fails to dissipate heat in response to thermal stress. It was first described by Roman in 84 BC, but only in 1940, it was recognized that heat stroke can result in multiorgan failure. Heat stroke is defined as a core body temperature usually in excess of 40ºC (104ºF) with associated central nervous system dysfunction in the setting of prolong environmental heat exposure. During high environmental heat exposure, blood flow to the skin increases many fold. However, when the ambient temperature is higher than the body’s core temperature, heat dissipating mechanism (conduction, convection and radiation) becomes ineffective. Environmental conditions also effect evaporative cooling. A water vapor pressure gradient is basic requisite to sweat; to evaporate and release heat, into the environment. In high

“Heat not the furnace for your foes  So hot t hat it do singe yourself”                                   -William Shakespeare Human body normally generated enough heat to increase body temperature by 1˚ C every hour, however hypothalamic thermoregulatory system (thermostat), tightly regulates core body temperature to a precise set point of around 37˚C, with a fluctuation of about 0.5-1.0˚C. This is achieved through negative feedback mechanism regulating thermostat, and by dissipating excess heat from body, by conduction, convective, radiation and evaporation (sweating). Evaporation is the most effective method of heat dissipation. It involves water vaporization from skin and lung. The exact mechanism that determines, the absolute threshold body temperature, is not known, but it appears to be mediated by norepinephrine, dopamine, serotonin, acetylcholine, prostaglandin, and neuropeptides. FEVER VS HYPERTHERMIA - Elevation in body temperature could be due to fever or

"Bekhudi besabab nahi ghalib, Kuchh to hai jis ki pardadari hai"                               - Mirza Ghalib   Acute acalculous cholecystitis (AAC) is defined as acute necroinflammatory disease of gallbladder (GB), in the absence of cholelithiasis, and has multifactorial pathogenesis. It is clinically indistinguishable from acute calculous cholecystitis. AAC is the epiphenomenon (secondary manifestation) of various primary disease pathophysiology. It is typically seen in critically ill patients, though it is also reported in outpatient setting. PHYSIOLOGY OF BILIARY SYSTEM: Liver normally produces 600 ml bile per day (0.4 ml/min). Cholecystokinin (CCK) regulates functioning of this system. CCK release is stimulated by food bolus, which causes contraction and emptying of GB, relaxation of sphincter of Oddi, increased intestinal motility, and stimulation of pancreatic enzyme secretion. These all events allow normal emptying of GB to promote digestion .