Hypotonic hyponatremia (majority): check volume and urine sodiumĭiagnosis: If urine > 20 mEq/L probably renal losses (diuresis,ĬSW, adrenal insufficiency), if urine 20 mEq/L, urine osm > 100 Trauma or SAH patients at risk for vasospasm). SIADH: fluid restriction (800 cc/day, or volume expansion + loop diuretics in head.3% saline, PO salt tabs, consider fludrocortisone (0.1-0.4 mg/day) Eliminate free water (flushes, ½ NS in IV meds, etc.).CSW is hypovolemic, SIADH is hypervolemic.CSW is the key distinguishing factor (CSW is actually more common) SAH and traumatic brain injury are most likely to develop hyponatremia.Additionally, overzealous correction can lead to diffuse demyelinating lesions, pituitary damage, oculomotor nerve palsies, and CPM The major complication is metabolic encephalopathy which can lead to CNS pathology as well as ARDS. Mortality rates in hyponatremic patients are 2x that of their normonatremic cohort. Seen in 50% of hospitalized patients with neurologic problems, 40% of hospitalized AIDS patients, 4.5% of hospitalized elderly patients and 1% of all post-op patients. Volume (because urine (~ 75 mEq/L) < plasma) – you can’t just diurese because you will lose more free water than (replacement volume must be of lower sodium concentration than urine) Impaired, try combining furosemide with volume replacement Treatment: Most people will autocorrect but if renal Na excretion is Other causes: mannitol, contrast, hyperglycemia, fluid overloadĬauses: hypertonic saline resuscitation, bicarbonate infusion, etc.Replace fluids lost with ½ NS + KCl at mL:mL ![]() Treatment: DDAVP IV at 0.5 – 2.0 g per dose, q4h, q6h Osm, target serum 150-155 mEq/L in 24h.Diagnosis: urine250 cc/hr, normal/high serum mOsm.Incidence: 6.7% in post-craniotomy (tumor), 4% after aneurysm, 2% after TBI.Diabetes Insipidus in the Neurosurgical Patientĭiabetes Insipidus in the Neurosurgical Patient If DI is not the problem it is most likely a fluid management problem. Again, correct free water using the TBW deficit equation (over the course of 2-3 days) and if the etiology is central, give 2-5 U vasopressin SQ q4-6h and monitor closely. Treatment: once diagnosed, administer 5 U vasopressin IV. This is a dangerous test and these patients must be To diagnose DI, fluid restrict and watch over the nextįew hours – if urine osmolality does not increase by 30 mOsm/L,ĭiagnose DI. Pressures, cardiac output, or the “shock variables.” After volume hasīeen corrected, tonicity can be corrected with free waterĬauses: nephrogenic DI is caused by hypokalemia, aminoglycosides,ĭiagnosis: urine < 200 mOsm/L in central and 200 – 500 in Volume replacement should should be guided by filling In this setting may have a mortality rate as high as 50%. Hypertonicity is metabolic encephalopathy (seizures, FND, coma) which May not be apparent because of the hypertonicity. Other: Hypovolemia is the most immediate threat (hypoperfusion) but Treatment: rapidly replace volume (NS vs 5% albumin), slowly replaceįree water (deficit (L) = x ), 50%Īcutely and the remainder over 24-36 hours to minimize cerebral ![]() Hypovolemic hyperntremia (most common in general ICU’s):Ĭauses: loss of hypotonic body fluids (diuresis, diarrhea, vomiting) If these are not available, look to clinical variables such as 1) weight loss 2) peripheral edema 3) urine (< 10 mEq/L suggests decreased ECV) and lastly the “shock variables” such as heart rate, blood pressure, urine output, and mental status. First, assess volume – if invasive hemodynamic monitoring is available, analyze the filling pressures and cardiac output.
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |