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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although a plethora of reports on life-threatening complications of salt emesis has been published since the early 1960s, salt is still used to induce emesis in cases of intoxication in the clinical as well as in the domestic setting. We report three cases of fatal hypernatremia after salt was used as an emetic. All fatalities were subjected to medico-legal autopsy at the Institute of Legal Medicine in Hamburg, Germany. In all cases, symptoms of cerebral damage such as seizures, fever and somnolence developed within hours after salt ingestion. All individuals were admitted to hospital before their deaths. Here, severe hypernatremia (up to 245 mmol/l) was detected, and all patients died under the clinical picture of cerebral edema despite intensive medical treatment. At autopsy, unspecific signs of a central regulatory failure were present. Histology revealed crenated red blood cells and few venous microthrombi in internal organs. Neuropathological investigations yielded no specific results but confirmed fatal cerebral edema and excluded other cerebral causes of death. Viewing the results of clinical and post-mortem investigations together, death could clearly be attributed to excessive salt intake in all cases.
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PMID:Fatal hypernatremia after using salt as an emetic--report of three autopsy cases. 1555 15

This was a retrospective study to assess the clinical profile of children admitted with acute renal failure and to identify factors associated with poor outcome. Fifty-four children (age one month to 12 years) with acute renal failure were studied. Males outnumbered females (38/54; 70%). The leading precipitating causes for renal failure were acute gastro-enteritis (85%), underlying renal pathology (43%), proven sepsis (22%) and suspected sepsis (22%). The main presenting complaints were diarrhoea (86%),oliguria (72%), rapid respiration (37%), oedema (37%), vomiting (19%) and seizures (13%). All patients underwent standard investigations and treatment. Forty-eight per cent of patients required peritoneal dialysis and 15% required ventilation. The overall mortality was 52%. Underlying renal pathology and sepsis both contributed to the high morbidity and mortality. Mortality due to sepsis was 83%; it was 65% in dialysed patients and 100% in those requiring ventilatory support. Biochemical profile of the above patients showed that hyperkalaemia was significantly associated with high mortality (83%) as against 75% in those with hypokalaemia and 33% with normal levels (p<0.001). Patients with hyponatraemia and hypernatraemia similarly had an adverse outcome. Acidosis, seen in 20 patients, had a mortality of 45%. The outcome was poorer in those with high creatinine levels (63%).
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PMID:Clinical profile and outcome of acute renal failure in South Indian children. 1571 79

Dehydration is commonly but often inappropriately diagnosed in cancer patients. Dehydration is the loss of water from the intracellular compartment due to hypernatremia. Dehydration can occur among patients who are hypervolemic, euvolemic, or hypovolemic. Cancer patients are more often hypovolemic, reflecting depletion of water from the extracellular space due to excessive loss, such as from vomiting and diarrhea, or inadequate intake of fluids. Hypovolemia can be hypernatremic, eunatremic, or hyponatremic. The appropriate state of the patient should be determined prior to attempts at correcting the problem. A hyponatremic patient would rehydrate more quickly with a solution higher in sodium, whereas this solution could be dangerous for a hypernatremic patient. Rapid or inappropriate treatment of hypernatremia can lead to death. Subjective findings, physical findings, and laboratory values will help direct the appropriate resuscitation methods. This paper reviews the physiologic control of extracellular volume and electrolytes, diagnosis of sodium and water balance problems, and the management of these concerns.
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PMID:Hypovolemia and dehydration in the oncology patient. 1708 Jul 33

A 9-year-old girl was admitted for the treatment of hyper-natremic dehydration. Her history was significant for psychogenic polydipsia, hyponatremia, and a renal concentrating defect. She presented with a 2-day history of altered mental status, ataxia, lethargy, fever, nausea, vomiting, and diarrhea. Meningitis was ruled out. Over the course of her illness, slow rehydration was maintained with a gradual decrease (10 mEq per 24 hours) of the serum sodium. Despite this care, she developed quadriparesis, and magnetic resonance imaging performed on day 6 of her illness was consistent with osmotic demyelination (central pontine myelinolysis). To rule out an excessively rapid correction of hypernatremia as the etiology of the problem, a myelin basic protein was measured in the cerebrospinal fluid that had been obtained on hospital day 1. The myelin basic protein was 649.50 ng/mL (normal, 0.07-4.10 ng/mL). The current literature is presented regarding the postulated pathogenesis of central pontine myelinolysis and suggested therapies, previous reports of central pontine myelinolysis in children are reviewed, and the potential role of myelin basic protein in its diagnosis is discussed.
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PMID:Osmotic demyelination and hypertonic dehydration in a 9-year-old girl: changes in cerebrospinal fluid myelin basic protein. 1709 2

1. The kidneys are the key organs to maintain the balance of the different electrolytes in the body and the acid-base balance. Progressive loss of kidney function results in a number of adaptive and compensatory renal and extrarenal changes that allow homeostasis to be maintained with glomerular filtration rates in the range of 10-25 ml/min. With glomerular filtration rates below 10 ml/min, there are almost always abnormalites in the body's internal environment with clinical repercussions. 2. Water Balance Disorders: In advanced chronic kidney disease (CKD), the range of urine osmolality progressively approaches plasma osmolality and becomes isostenuric. This manifests clinically as symptoms of nocturia and polyuria, especially in tubulointerstitial kidney diseases. Water overload will result in hyponatremia and a decrease in water intake will lead to hypernatremia. Routine analyses of serum Na levels should be performed in all patients with advanced CKD (Strength of Recommendation C). Except in edematous states, a daily fluid intake of 1.5-2 liters should be recommended (Strength of Recommendation C). Hyponatremia does not usually occur with glomerular filtration rates above 10 ml/min (Strength of Recommendation B). If it occurs, an excessive intake of free water should be considered or nonosmotic release of vasopressin by stimuli such as pain, anesthetics, hypoxemia or hypovolemia, or the use of diuretics. Hypernatremia is less frequent than hyponatremia in CKD. It can occur because of the provision of hypertonic parenteral solutions, or more frequently as a consequence of osmotic diuresis due to inadequate water intake during intercurrent disease, or in some circumstance that limits access to water (obtundation, immobility). 3. Sodium Balance Disorders: In CKD, fractional excretion of sodium increases so that absolute sodium excretion is not modified until glomerular filtration rates below 15 ml/min (Strength of Recommendation B). Total body content of sodium is the main determinant of extracellular volume and therefore disturbances in sodium balance will lead to clinical situations of volume depletion or overload: Volume depletion due to renal sodium loss occurs in abrupt restrictions of salt intake in advanced CKD. It occurs more frequently in certain tubulointerstitial kidney diseases (salt losing nephropathies). Volume overload due to sodium retention can occur with glomerular filtration rates below 25 ml/min and leads to edema, arterial hypertension and heart failure. The use of diuretics in volume overload in CKD is useful to force natriuresis (Strength of Recommendation B). Thiazides have little effect in advanced CKD. Loop diuretics are effective and should be used in higher than normal doses (Strength of Recommendation B). The combination of thiazides and loop diuretics can be useful in refractory cases (Strength of Recommendation B). Weight and volume should be monitored regularly in the hospitalized patient with CKD (Strength of Recommendation C). 4. Potassium Balance Disorders: In CKD, the ability of the kidneys to excrete potassium decreases proportionally to the loss of glomerular filtration. Stimulation of aldosterone and the increase in intestinal excretion of potassium are the main adaptive mechanisms to maintain potassium homeostasis until glomerular filtration rates of 10 ml/min. The main causes of hyperkalemia in CKD are the following: Use of drugs that alter the ability of the kidneys to excrete potassium: ACEIs, ARBs, NSAIDs, aldosterone antagonists, nonselective beta-blockers, heparin, trimetoprim, calcineurin inhibitors. Determination of serum potassium two weeks after the initiation of treatment with ACEIs/ARBs is recommended (Strength of Recommendation C). Routine use of aldosterone antagonists in advanced CKD is not recommended (Strength of Recommendation C). Abrupt reduction in glomerular filtration rate: Constipation. Prolonged fasting. Metabolic acidosis. A low-potassium diet is recommended with GFR less than 20 ml/min, or GFR less than 50 ml/min if drugs that raise serum potassium are taken (Strength of Recommendation C). In the absence of symptoms or electrocardiographic abnormalities, review of medications, restriction of dietary potassium and use of oral ion exchange resins are usually sufficient therapeutic measures (Strength of Recommendation C). If symptoms and/or electrocardiographic abnormalities are present, the usual parenteral pharmacological measures should be used (10% calcium gluconate, insulin and glucose, salbutamol, resins, diuretics) (Strength of Recommendation A). Parenteral bicarbonate and ion exchange resins in enemas are not recommended as first-line treatment (Strength of Recommendation C). Hemodialysis should be considered in patients with glomerular filtration rates below 10 ml/min (Strength of Recommendation C). 5. Acid-Base Disorders in CKD: Moderate metabolic acidosis (Bic 16-20) mEq/L is common with glomerular filtration rates below 20 ml/min, and favors bone demineralization due to the release of calcium and phosphate from the bone, chronic hyperventilation, and muscular weakness and atrophy. Its treatment consists of administration of sodium bicarbonate, usually orally (0.5-1 mEq/kg/day), with the goal of achieving a serum bicarbonate level of 22-24 mmol/L (Strength of Recommendation C). Limitation of daily protein intake to less than 1 g/kg/day is also useful (Strength of Recommendation C). Use of sevelamer as a phosphate binder aggravates metabolic acidosis since it favors endogenous acid production and therefore acidosis should be monitored and corrected if it occurs (Strength of Recommendation C). Hypocalcemia should always be corrected before metabolic acidosis in CKD (Strength of Recommendation B). Metabolic acidosis is an infrequent disorder and requires exogenous alkali administration (bicarbonate, phosphate binders) or vomiting.
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PMID:[Electrolyte and acid-base balance disorders in advanced chronic kidney disease]. 1901 44

An 87-year-old male, prescribed digoxin and furosemide for congestive heart failure and Alzheimer disease, had dehydration and anemia due to poor food intake and hemorrhagic cystitis. Repeated vomiting due to an upper respiratory infection caused disturbance of consciousness and hypotension. The patient was admitted to hospital and diagnosed with digoxin intoxication and hypernatremia. The serum sodium (Na(+)) level was corrected, but the patient died 4 days after admission following uncontrollable seizure. A histologic examination after an autopsy revealed characteristic findings of central pontine myelinolysis (CPM). This is the first autopsy report on CPM triggered by vomiting in association with digoxin administration.
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PMID:Autopsy report on central pontine myelinolysis triggered by vomiting associated with digoxin intoxication. 1978 35

A 6-month-old miniature Schnauzer presented with hypernatremia and clinical signs of vomiting, diarrhea, inappetence, and lethargy. The dog did not consume water on its own. Hypernatremia and the related clinical signs were resolved by fluid administration. Endocrinological investigations and urinalysis excluded the possibility of diabetes insipidus and hyperaldosteronism. Therefore, the dog was diagnosed with hypodipsic hypernatremia. Magnetic resonance imaging revealed dysgenesis of the corpus callosum and other forebrain structures. On the basis of these findings, congenital brain malformation associated with failure of the osmoreceptor system was suspected.
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PMID:Magnetic resonance imaging and clinical findings in a miniature Schnauzer with hypodipsic hypernatremia. 1988 48

We report a 20-year-old man who presented to our emergency room with a history of polyuria, weakness, constipation, nausea, and vomiting of two months duration. History and clinical examination revealed a significant weight loss and mild hepatomegaly. Laboratory investigations revealed hypokalemia, hypernatremia, and severe metabolic acidosis and anemia. Ultra-sound of the abdomen revealed enlarged kidneys without hydronerphrosis. The patient developed paralysis due to further decline in serum potassium level, which improved after an aggressive fluid and electrolyte management. He was investigated extensively for polyuria and type of acidosis. The kidney biopsy showed interstitial leukemic infiltration. He was managed accordingly and recovered from the condition. This case demonstrates an unusual presentation of a hematological malignancy, which was a diagnostic as well as a management challenge.
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PMID:A young man with polyuria and lethargy. 2174 47

Diabetes insipidus is a rare endocrine disorder in paediatric patients. Polyuria is a cardinal manifestation that is extremely difficult to recognize in diapered infants. Careful urine quantification is the key to diagnosis in appropriate clinical setting. We report a case of a 4 months old infant presenting with an acute life threatening event following an episode of vomiting and decreased oral intake. She had profound hypernatremia which persisted after stabilization. Polyuria unrecognized by the mother was revealed by 24-hour urine output measurement. A diagnosis of diabetes insipidus was made after appropriate laboratory investigations including serum and urine osmolality. The central nature of the disease was confirmed by neuroimaging which showed holoprosencephaly.
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PMID:Profound hypernatremia due to central diabetes insipidus. 2263 Jan 7

A 9-year-old boy presented with feeding and behavioural problems and was diagnosed with Autistic Spectrum Disorder and Attention Deficit Hyperactivity Disorder. By age 11 he was becoming increasingly disinhibited and was refusing almost all oral food intake. Believing the cause to be psychogenic, he was placed in an inpatient eating disorder facility. After 3 days of continuous vomiting and minimal intake, he was admitted back to hospital for further investigations. A hypovolaemic hypernatraemia prompted an MRI brain scan, revealing several tumour masses with suprasellar and pituitary involvement. Histological investigation revealed primary, non-malignant germ-cell tumours. The tumours were treated with craniopharyngeal radiotherapy and permanent pituitary hormone replacement.
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PMID:An unusual suspect causing behavioural problems and pituitary failure in a child. 2324 80


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