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severity of DKA

severity of DKA

As a rough gradation, the following benchmarks can be helpful:(32771260, British guidelines)

Severe DKA: serum bicarbonate <5 mM (or pH < 7.0-7.1, or beta-hydroxybutyrate >6 mM).

Moderate DKA: serum bicarbonate 5-10 mM (or pH ~7.1-7.2).

Mild DKA: serum bicarbonate >10 mM (or pH >7.2).

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DKA/Diabetes Ketoacidosis

Three ways to evaluate for ketoacidosis ( from IBCC)

(#1) anion gap

Anion Gap = (Na – Cl – Bicarbonate)

Using this formula, an elevated anion gap is above 10-12 mEq/L.(23833313)

Please don't correct for albumin, glucose, or potassium. Don't make this unnecessarily complicated.

Anion gap may be elevated due to a variety of causes (with the differential diagnosis explored here). Therefore, an elevated anion gap does not necessarily imply DKA! This is especially true among patients with chronic renal failure, who may have a chronically elevated anion gap.

(#2) urinary dipstick for ketones

The urinary ketone dipstick tests for acetoacetate.

This test has a high sensitivity for DKA (98-99%), with urinary ketones are generally being ≧2+.(32771260, 10459090) False negatives may occur in patients with highly acidic urine.(32409703)

The specificity of a positive measurement of urinary ketones is low, so a positive urinary measurement of ketones doesn't establish a diagnosis of DKA.(32763063) For example, starvation ketoacidosis is a more common cause of urinary ketones in most contexts.

(#3) blood beta-hydroxybutyrate level

Beta-hydroxybutyrate level is the gold standard for defining the presence and extent of ketoacidosis in DKA.

Rough interpretation:(32771260)

0-0.6 mM: Normal

0.6-1 mM: Mild ketosis, may consider adjustment of insulin regimen. Among patients who initially presented with DKA, a reduction of the beta-hydroxybutyrate level below <1 mM indicates resolution of the DKA.(32409703)

1-3 mM: Moderate ketosis, medical intervention is warranted. There is a risk of progression to DKA.

>3 mM: Consistent with DKA.(10030312, 18184896, 32771260)

>6 mM: Severe DKA.

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Bicarbonate Therapy

Bicarbonate Therapy

In all cases, the primary goal in treating metabolic acidosis is to focus on reversal of the underlying process causing the acidosis.  Examples:  (1) Renal failure: dialysis if needed. (2) Alcoholic ketoacidosis: fluids, electrolytes, thiamine, folic acid.  (3) Sepsis/shock: volume resuscitation, vasopressors, etc.  (4) Salicylate intoxication:  IV fluids, alkalinization of the urine, ....   

If there is a severe deficit (HCO3- < 10-12 mEq/L and pH<7.2) correct with sodium bicarbonate.    Sodium bicarb is also useful if the acidosis is due to inorganic acids (especially if renal disease is present).  However, when the acidosis results from organic acids (lactic acid, acetoacetic acid, etc) the role of bicarbonate is controversial.  In most cases of DKA or severe lactic acidosis the administration of sodium bicarbonate does not decrease mortality even when the acidosis is severe.  In sum, sodium bicarbonate should be reserved for severe cases of acidosis only (pH <7.2 and serum bicarbonate levels <10-12 meq/L).  This can be accomplished by adding 1 to 3 ampoules of sodium bicarb to D5W or 1/2NS.   IV-push administration should be reserved for cardiac life support and not metabolic acidosis.

Sodium bicarbonate administration: It is recommended that 50% of total deficit be given over 3 to 4 hours, and the remainder replaced over 8-24 hours. The usual initial target ((desired HCO3- concentration): 10 - 12 mEq/L, which should bring the blood pH to ~7.20. The subsequent goal is to increase the bicarbonate level to 15 meq/L over the next 24 hours.

Koda-Kimble et al: Replace 50% over 3 to 4 hours and the reminder over 24 hours.  Once the pH is 7.2 - 7.25, the serum [HCO3-] should not be increased by more than 4 to 8 mEq/L over 6 to 12 hours to avoid the risks of over-alkalinization (paradoxical CNS acidosis; decreased affinity of hemoglobin for oxygen leading to tissue hypoxia and lactic acid production; sodium overload; and hypokalemia).

Bicarb Vd = (0.4 + 2.6/HCO3-) x Lean body weight.

Bicarbonate deficit = Bicarb Vd x (desired [HCO3-] - measured [HCO3-])

Lean body weight defined as usual IBW equations: Estimated ideal body weight in (kg): Males: IBW = 50 kg + 2.3 kg for each inch over 5 feet. Females: IBW = 45.5 kg + 2.3 kg for each inch over 5 feet.

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Bicarbonate Deficit calculation

Bicarbonate Deficit calculation formula

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5 posts!

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Brain Death New Protocol 2023

Pediatric and Adult Brain Death/Death by Neurologic Criteria Consensus Guideline | Neurology

Pediatric and Adult Brain Death/Death by Neurologic Criteria Consensus Guideline

Report of the AAN Guidelines Subcommittee, AAP, CNS, and SCCM

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DT and Mortality

Mortality — With early identification and appropriate management, mortality from DT is less than 5 percent. This figure has fallen from the 37 percent mortality rate reported in the early 20th century, probably as a result of earlier diagnosis, improvements in supportive and pharmacologic therapies, and improved treatment of comorbid illnesses [4,28-32]. Death usually is due to dysrhythmia, complicating illnesses such as pneumonia, or failure to identify an underlying problem that led to the cessation of alcohol use, such as pancreatitis, hepatitis, or central nervous system injury or infection. Older age, pre-existing cardiopulmonary disease, core body temperature greater than 40ºC (104ºF), and coexisting liver disease are associated with a greater risk of mortality .

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Malignant cerebral hemispheric infarction with swelling and risk of herniation: UTD

Osmotic and salvage therapies — Acute cerebral edema with life-threatening mass effect can be treated, at least temporarily, with hypertonic saline, mannitol, or hyperventilation. These interventions are most effective when used as a bridging therapy to decompressive hemicraniectomy [3], and are not intended for prolonged use. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Osmotic therapy and diuresis'.)

●Intravenous mannitol quickly and effectively lowers intracranial pressure. Mannitol regimens vary between institutions and regions. It is most common to start with a bolus of 1 to 1.5 g/kg of mannitol 20 percent. Subsequent doses may be scheduled (eg, 0.5 g/kg every 6 hours) or given as needed for signs of clinical decline or radiologic progression. Patients receiving repeated doses of mannitol should have their serum osmolality and osmolar gap monitored to avoid nephrotoxicity; the risk is high when serum osmolality increases above 320 milliosmoles/kg and when the osmolar gap is greater than 20. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Osmotic therapy and diuresis' and "Complications of mannitol therapy".)

●Hypertonic saline is an effective hyperosmolar agent for lowering intracranial pressure. Bolus doses of various concentrations (from 3 to 23.4 percent) and volumes (most commonly 50 mL of 14 percent or 30 mL of 23.4 percent sodium chloride) can be administered. (See "Management of acute moderate and severe traumatic brain injury", section on 'Osmotic therapy'.)

●Hyperventilation causes a rapid lowering of intracranial pressure by inducing cerebral vasoconstriction, but the effect is short-lived. Brief hyperventilation may be used as a bridge to more definitive therapy for deteriorating patients with signs of brainstem herniation [3,46]. A partial pressure of carbon dioxide (PaCO2) goal of 30 to 35 mmHg is suggested. More aggressive (ie, a PaCO2 goal of 26 to 30 mmHg) or prolonged hyperventilation may result in brain ischemia and worse outcomes.

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Alcohol withdrawal BDZ management UTD

Diazepam>> Lorazepam >> Midazolam

Benzodiazepam for alcohol withdrawal

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Albumin in the Critical care

1.Albumin is recommended for the diagnosis and treatment of Type 1 hepatorenal syndrome with cirrhosis 2. Albumin is recommended for the treatment of spontaneous bacterial peritonitis with cirrhosis in conjunction with appropriate antimicrobial therapy 3. Repletion with albumin is recommended after large volume paracentesis in cirrhosis and after plasmapheresis 4. General use of albumin to treat all patients with sepsis is not recommended, however albumin may be considered for the treatment of septic and hemorrhagic shock following failure of isotonic crystalloid fluids 5. Albumin may be considered in patients that are edematous but intravascularly depleted and with a plasma albumin <2 g/dL. Examples populations include patients with cirrhosis that have ascites that is unresponsive to diuretics and who are not undergoing paracentesis OR patients who have undergone major surgery (e.g. > 40% hepatic resection or extensive intestinal resection) 6. Use of albumin may be considered to treat burns when appropriate administration of crystalloid fluid does not result in minimum urine output. 7. Albumin may be considered to treat volume depletion following liver transplant 8. Albumin may be considered for treatment of hypo-oncotic shock in patients with acute respiratory distress syndrome 9. Albumin may be considered to treat diuretic resistance 10. Albumin may be considered to treat symptomatic hypotension during hemodialysis 11. Albumin should not be administered to patients with traumatic brain injury and should be administered with care in the setting of other traumas.