Renal Failure after Accidental Hypothermia

McKean, W. I.; Dixon, S. R.; Gwynne, J. F.; Irvine, R.O.H.

doi:10.1136/bmj.2.5707.463

Cited by 16 publications

(4 citation statements)

References 3 publications

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“…Raised serum amylase levels are commonly found in patients with accidental hypothermia (Duguid et al, 1961;Holmes and Emslie-Smith, 1961;Read et al, 1961;Prescott et al, 1962;Murphy and Faul, 1963;Jones et al, 1966;McKean et al, 1970). Such high levels, usually reverting to normal in about a week Murphy and Faul, 1963), may be found without the usual clinical manifestations of acute pancreatitis which occur in euthermic patients (Jones et al, 1966).…”

Section: Introductionmentioning

confidence: 99%

Acute Pancreatitis and Diabetic Ketoacidosis in Accidental Hypothermia and Hypothermic Myxoedema

Maclean¹,

Murison²,

Griffiths³

1973

BMJ

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Section: Introductionmentioning

confidence: 99%

Acute Pancreatitis and Diabetic Ketoacidosis in Accidental Hypothermia and Hypothermic Myxoedema

Maclean¹,

Murison²,

Griffiths³

1973

BMJ

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“…Rewarming from deep accidental hypothermia can be complicated by renal failure (1, 2). Although posthypothermic renal complications have received little emphasis in most clinical case reports, they are by no means uncommon (3).…”

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confidence: 99%

Morphologic changes in tubular cells from in situ kidneys following experimental hypothermia and rewarming

Tveita

Johansen

Lien

et al. 2005

APMIS

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Although renal failure may occur following rewarming from deep accidental hypothermia, this subject has received little attention in experimental hypothermia and clinical case reports. In order to explore the integrity of hypothermic and posthypothermic renal morphology we used an experimental animal model of accidental hypothermia where the heart supports the circulation throughout cooling and rewarming without accompanying cardioplegia or ischemia. Ultrastructural changes in renal tubular cells from three groups of pentobarbital anesthetized Wistar rats: 1) controls (n=6) maintained at 37 degrees C for 4 h, 2) hypothermic rats (n=6) core-cooled and maintained at 15-13 degrees C for 4 h, and 3) rewarmed rats (n=10), were studied as a sensitive indicator of renal damage. Electron micrographs (EM) from hypothermic kidneys showed rounded up mitochondria with loss of contrast. These changes were observed in several though not all of the biopsies, but they were found in all kidneys. Areas exhibiting focal tubular necrosis were seen on most EM from three of these kidneys. EM from rewarmed kidneys showed alterations of mitochondrial ultrastructure with similarities to those observed after hypothermia, but in general the changes were more prominent. Extracellular edema, intracellular edema, swelling of mitochondria, margination of chromatin, necrosis of single tubular cells, and disrupting necrotic debris into tubular lumen could be found in micrographs from 7 of the 10 kidneys examined. Rewarming from experimental hypothermia, without episodes of ischemia or hypoxia, thus induces ultrastructural changes in renal tubular cells similar to changes observed in acute tubular necrosis, associated with renal failure.

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“…Nelle fasi più avanzate il filtrato glomerulare diminuisce, parallelamente al calo della portata cardiaca, con riduzione anche della funzione tubulare, inclusa la capacità di secernere idrogenioni con conseguente acidosi. Una franca insufficienza renale con rilievo istologico di lesioni ischemiche e necrosi tubulare è presente in quasi la metà dei casi di ipotermia [19,20]. Iperglicemia può essere osservata sia a causa della ridotta funzionalità insulare sia come conseguenza dell'attivazione catecolaminica e corticosurrenalica [21,22].…”

Section: Effetti Renali E Metaboliciunclassified

Hypotermia in the elderly

et al. 2012

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IntroductionAn 88-year-old woman suffered a cerebrovascular accident and was found on the floor of her cold house.Materials and methodsAt the time of admission to our division, the patient was unresponsive with a rectal temperature of 28 °C, blood pressure of 120/80 mmHg, and a heart rate of 40 bpm. The cerebral CT revealed a hypodense lesion in the temporal region. The ECG showed sinus bradycardia, prolonged PR and QTc intervals, and a classic “J” (Osborn) wave that was most pronounced in the lateral and inferior leads. The patient presented a low respiratory rate, hypoventilation, severe acidosis (both respiratory and metabolic), hyperkalemia, elevated liver enzymes, mild anemia, hyporeflexia, and sluggish pupil responses.ResultsDuring rewarming with thermic blanket and heated intravenous fluids, the respiratory condition improved, and the ECG alterations disappeared. Twenty-four hours later, however, the patient died suddenly due to cardiac asystole.DiscussionThis report analyses the effects of hypothermia and its clinical manifestations and provides a brief discussion of the electrophysiologic mechanisms underlying Osborn waves and the other electrocardiographic changes associated with hypothermia.

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Renal Failure after Accidental Hypothermia

Cited by 16 publications

References 3 publications

Acute Pancreatitis and Diabetic Ketoacidosis in Accidental Hypothermia and Hypothermic Myxoedema

Acute Pancreatitis and Diabetic Ketoacidosis in Accidental Hypothermia and Hypothermic Myxoedema

Morphologic changes in tubular cells from in situ kidneys following experimental hypothermia and rewarming

Hypotermia in the elderly

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