Abstract:We present a case of a 29-year-old woman with known Type 1 diabetes who presented with diabetic ketoacidosis (DKA). Despite appropriate treatment and initial improvement, 12 h after initiation of treatment she deteriorated rapidly and developed pulmonary oedema, cerebral oedema and multiple infarctions of the brain and cervical spinal cord. This resulted in spastic quadraparesis and she has remained wheelchair-bound. These complications of DKA are rare and unpredictable. In this case report we discuss the prop… Show more
“…As with cerebral oedema, the observation that pulmonary oedema usually occurs within a few hours of initiation of treatment has led to the speculation that the complication is iatrogenic and that rapid infusion of crystalloids over a short period of time increases the likelihood of this complication [48]. Elderly patients and those with impaired cardiac function are at particular risk and monitoring of central venous pressure should be considered.…”
The Joint British Diabetes Societies guidelines for the management of diabetic ketoacidosis (these do not cover Hyperosmolar Hyperglycaemic Syndrome) are available in full at: This article summarizes the main changes from previous guidelines and discusses the rationale for the new recommendations. The key points are: Monitoring of the response to treatment (i) The method of choice for monitoring the response to treatment is bedside measurement of capillary blood ketones using a ketone meter.(ii) If blood ketone measurement is not available, venous pH and bicarbonate should be used in conjunction with bedside blood glucose monitoring to assess treatment response.(iii) Venous blood should be used rather than arterial (unless respiratory problems dictate otherwise) in blood gas analysers.(iv) Intermittent laboratory confirmation of pH, bicarbonate and electrolytes only.Insulin administration (i) Insulin should be infused intravenously at a weight-based fixed rate until the ketosis has resolved.(ii) When the blood glucose falls below 14 mmol ⁄ l, 10% glucose should be added to allow the fixed-rate insulin to be continued.(iii) If already taking, long-acting insulin analogues such as insulin glargine (Lantus Ò
“…As with cerebral oedema, the observation that pulmonary oedema usually occurs within a few hours of initiation of treatment has led to the speculation that the complication is iatrogenic and that rapid infusion of crystalloids over a short period of time increases the likelihood of this complication [48]. Elderly patients and those with impaired cardiac function are at particular risk and monitoring of central venous pressure should be considered.…”
The Joint British Diabetes Societies guidelines for the management of diabetic ketoacidosis (these do not cover Hyperosmolar Hyperglycaemic Syndrome) are available in full at: This article summarizes the main changes from previous guidelines and discusses the rationale for the new recommendations. The key points are: Monitoring of the response to treatment (i) The method of choice for monitoring the response to treatment is bedside measurement of capillary blood ketones using a ketone meter.(ii) If blood ketone measurement is not available, venous pH and bicarbonate should be used in conjunction with bedside blood glucose monitoring to assess treatment response.(iii) Venous blood should be used rather than arterial (unless respiratory problems dictate otherwise) in blood gas analysers.(iv) Intermittent laboratory confirmation of pH, bicarbonate and electrolytes only.Insulin administration (i) Insulin should be infused intravenously at a weight-based fixed rate until the ketosis has resolved.(ii) When the blood glucose falls below 14 mmol ⁄ l, 10% glucose should be added to allow the fixed-rate insulin to be continued.(iii) If already taking, long-acting insulin analogues such as insulin glargine (Lantus Ò
“…During our literature search, we found only one other published case report, by Dixon et al 1 where a patient developed pulmonary and cerebral oedema and also multiple CNS infarctions including the spinal cord. We also found reports of cerebral oedema in children with DKA but without spinal cord oedema 2 3…”
Section: Discussionmentioning
confidence: 97%
“…The existing theories are limited to cerebral oedema and are mostly in the paediatric diabetic population. However, the pathophysiology behind cerebral oedema and infarction is not clear and there are a few existing theories in the literature, such as: systemic hypotension and hypoxia, rapid changes in serum osmolarity, disseminated intravascular coagulation and thrombosis secondary to dehydration, haemoconcentration and hyperviscosity 1 3 4…”
A 23-year-old man with poorly controlled insulin-dependent diabetes mellitus presented to casualty with community-acquired pneumonia and diabetic ketoacidosis. Shortly after admission he deteriorated and developed cardiac failure, pulmonary oedema and further decreased level of consciousness. He was sedated and ventilated for 3 weeks in the intensive care unit. On waking from sedation he was found to be tetraplegic. MRI scan showed gross oedema of the cervical spinal cord with area suspicious of infarction. We describe a rare cause of spinal cord injury and discuss the proposed hypotheses.
“…However, DKA associated with stroke in adults remains rare 8. On review of the literature, there are only a small number of case reports regarding the development of ischaemic stroke in adult patients with DKA 8 – 10.…”
SUMMARYA 34-year-old man presented to a hospital with a 7-day history of nausea, vertigo, ataxia and frontal headache. Examination revealed ipsilateral cerebellar signs. CT of the brain demonstrated left cerebellar hypodensity suggestive of ischaemic stroke or space occupying lesion. Full blood count showed a markedly raised haemoglobin (219 g/L) and haematocrit (0.56). Admission urinalysis was performed but the results not reviewed. Owing to patient deterioration, an arterial blood gas was performed. This showed profound metabolic acidosis. Repeat urinalysis was positive for glucose and ketones. MRI of the brain confirmed ischaemic stroke. The underlying cause of this was hyperviscosity secondary to relative polycythaemia, resulting from undiagnosed diabetic ketoacidosis as a first presentation of diabetes. This case report highlights ischaemic stroke as an unusual presenting feature of diabetic ketoacidosis. Notably, the underlying diagnosis of diabetic ketoacidosis was initially missed, thereby emphasising the importance of performing an admission urinalysis and acting on the results.
BACKGROUND
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.