Hyperventilation in severe diabetic ketoacidosis*

Tasker, Robert C.; Lutman, Daniel; Peters, Mark

doi:10.1097/01.pcc.0000164343.20418.37

Cited by 50 publications

(22 citation statements)

References 36 publications

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“…Conversely, when patients are spontaneously hyperventilating to lower PaCO 2 levels, ventilating them at normal levels may be detrimental as well (75). Patients with symptomatic CE who are intubated should probably be ventilated to PaCO 2 levels existing at the time intubation is performed (75)(76)(77)(78)(79)(80).…”

Section: Therapy Of Cerebral Edema In Diabetic Ketoacidosismentioning

confidence: 98%

“…This is consistent with the theory that low PaCO 2 levels cause vasoconstriction and ischemic injury to the blood-brain barrier, resulting in vasogenic edema. Tasker et al (75) argued that patients who are intubated and ventilated for symptomatic CE need to be ventilated at PaCO 2 levels lower than the normal range, because ventilation at normal PaCO 2 levels represents a sudden increase in patients' PaCO 2 from their spontaneous hyperventilation state during DKA and has detrimental effects. Fortune (76), Marcin et al (77), and Ackerman (78) seem to agree with this, suggesting that patients intubated and ventilated for CE should be ventilated to PaCO 2 levels representing their baseline state at the onset of symptoms to avoid either too high or too low PaCO 2 levels.…”

Section: Pathophysiology and Risk Factorsmentioning

confidence: 99%

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Cerebral edema in diabetic ketoacidosis

Levin¹

2008

Pediatric Critical Care Medicine

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The causes and mechanisms of CEDKA are unknown. CEDKA may be due as much to individual biological variance as to severity of underlying metabolic derangement of the child's state and/or treatment risk factors. Treatment recommendations for CEDKA and diabetic ketoacidosis are made taking into consideration possible mechanisms and risk factors but are intended as general guidelines only in view of the absence of conclusive evidence.

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Section: Therapy Of Cerebral Edema In Diabetic Ketoacidosismentioning

confidence: 98%

Section: Pathophysiology and Risk Factorsmentioning

confidence: 99%

Cerebral edema in diabetic ketoacidosis

Levin¹

2008

Pediatric Critical Care Medicine

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“…[37,38] Hyperventilation of intubated young patients with DKA has been shown to both improve and worsen outcomes. [39,40] …”

Section: Insulin Therapymentioning

confidence: 99%

Management of Diabetic Ketoacidosis in Children and Adolescents

Sherry

Levitsky

2008

Pediatric Drugs

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Diabetic ketoacidosis (DKA) is a life-threatening complication of diabetes mellitus. While it can occur in all types of diabetes mellitus, it is seen most often in patients with type 1 diabetes, either at presentation or as a result of non-compliance with medical therapy. DKA is characterized by hyperglycemia, acidosis, dehydration, and electrolyte abnormalities, which result from a deficiency of insulin and an excess of counter-regulatory hormones. Therapy is aimed at repleting fluids, and correcting acidosis and electrolyte disturbances by administration of intravenous fluid and intravenous insulin. Rapid correction should be avoided as it may result in untoward effects, including cerebral edema. Frequent monitoring of neurologic status and metabolic parameters aids in avoidance or early detection of complications. While much is still not understood about the most serious complication, cerebral edema, recent studies suggest that its development may be tied to a loss of cerebral autoregulation and a vasogenic mechanism of edema formation. Treatment of cerebral edema includes fluid restriction and administration of mannitol. Once DKA has resolved, subcutaneous insulin is initiated with careful consideration of its pharmacokinetics to avoid a period of insulin deficiency and metabolic decompensation.

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“…Whether the more frequent and greater duration of hyperventilation in the ICP group was also potentially detrimental is unknown. For example, at presentation, most patients with acute bacterial meningitis hyperventilate spontaneously (14), and we do not know what level in arterial CO 2 partial pressure should be targeted during mechanical ventilation in those with baseline hypocapnia (15). Normally, acute hyperventilation reduces CBF and CBV.…”

mentioning

confidence: 99%