HHS – full or prophylactic anticoagulation?

Wordsworth, Georgina; Robinson, Anthony; Ward, Alexandra; Atkin, Marc

doi:10.15277/bjdvd.2014.011

Cited by 4 publications

(3 citation statements)

References 8 publications

(10 reference statements)

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“…Unfortunately, there are no randomized trials comparing risk-benefit profile of prophylactic and full dose of LMWH. Case reports of thrombotic fatalities under prophylactic dose of LMWH may support the use of full LMWH dose in those with HHS and low hemorrhage risk [77]. Furthermore, Keenan et al demonstrated that thrombotic risk is increased for three months after discharge, with one third of venous thromboembolism events occurring in that period [75].…”

Section: Hypocoagulationmentioning

confidence: 96%

Controversies in the management of hyperglycaemic emergencies in adults with diabetes

et al. 2017

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Hyperglycaemic emergencies are associated with significant morbi-mortality and healthcare costs. Management consists on fluid replacement, insulin therapy, and electrolyte correction. However, some areas of patient management remain debatable. In patients without respiratory failure or haemodynamic instability, arterial and venous pH and bicarbonate measurements are comparable. Fluid choice varies upon replenishment phase and patient's condition. If patient is severely hypovolaemic, normal saline solution should be the first option. However, if patient has mild/moderate dehydration, fluid choice must take in consideration sodium concentration. Insulin therapy should be guided by β-hydroxybutyrate normalization and not by blood glucose. Variations of conventional insulin infusion protocols emerged recently. Priming dose of insulin may not be required, and fixed rate insulin infusion represents the best option to suppress hepatic glucose production, ketogenesis, and lipolysis. Concomitant administration of basal insulin analogues with regular insulin infusion accelerates ketoacidosis resolution and prevents rebound hyperglycaemia. Simpler protocols using subcutaneous rapid-acting insulin analogues for mild/moderate diabetic ketoacidosis treatment have proven to be safe and effective, but further studies are required to confirm these results. Treatment with bicarbonate, phosphate, and low-molecular-weight heparin is still disputable, and randomized controlled trials are urgently needed to optimize patient management and decrease the morbi-mortality of hyperglycaemic emergencies.

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Section: Hypocoagulationmentioning

confidence: 96%

Controversies in the management of hyperglycaemic emergencies in adults with diabetes

et al. 2017

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“…Whilst thrombotic complications such as myocardial infarction, stroke or peripheral arterial thrombosis occur more frequently in HHS, it is not known whether or not these can be prevented by prophylaxis with low dose LMWH or anti-platelet therapy, or if a full therapeutic dose should be used. 36,37 Having diabetes is associated with an increased risk of developing venous thromboembolic disease (VTE). 38 People with HHS have an increased risk of arterial and VTE.…”

Section: Anticoagulationmentioning

confidence: 99%

Section: Managementmentioning

confidence: 99%

Management of Hyperosmolar Hyperglycaemic State (HHS) in Adults: An updated guideline from the Joint British Diabetes Societies (JBDS) for Inpatient Care Group

et al. 2022

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Hyperosmolar Hyperglycaemic State (HHS) is a medical emergency associated with high mortality. It occurs less frequently than diabetic ketoacidosis (DKA), affects those with pre-existing/new type 2 diabetes mellitus and increasingly affecting children/younger adults. Mixed DKA/HHS may occur. The JBDS HHS care pathway consists of 3 themes (clinical assessment and monitoring, interventions, assessments and prevention of harm) and 5 phases of therapy (0-60 min, 1-6, 6-12, 12-24 and 24-72 h). Clinical features of HHS include marked hypovolaemia, osmolality ≥320 mOsm/kg using [(2×Na + ) + glucose+urea], marked hyperglycaemia ≥30 mmol/L, without significant ketonaemia (≤3.0 mmol/L), without significant acidosis (pH >7.3) and bicarbonate ≥15 mmol/L. Aims of the therapy are to improve clinical status/replace fluid losses by 24 h, gradual decline in osmolality (3.0-8.0 mOsm/kg/h to minimise the risk of neurological complications), blood glucose 10-15 mmol/L in the first 24 h, prevent hypoglycaemia/hypokalaemia and prevent harm (VTE, osmotic demyelination, fluid overload, foot ulceration). Underlying precipitants must be identified and treated. Interventions include: (1) intravenous (IV) 0.9% sodium chloride to restore circulating volume (fluid losses 100-220 ml/kg, caution in elderly), (2) fixed rate intravenous insulin infusion (FRIII) should be commenced once osmolality stops falling with fluid replacement unless there is ketonaemia (FRIII should be commenced at the same time as IV fluids). (3) glucose infusion (5% or 10%) should be started once glucose <14 mmol/L and (4) potassium replacement according to potassium levels. HHS resolution criteria are: osmolality <300 mOsm/kg, hypovolaemia corrected (urine output ≥0.5 ml/kg/h), cognitive status returned to pre-morbid state and blood glucose <15 mmol/L.

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Mesenteric venous thrombosis: A lethal complication of hyperglycemic crises

Tsai

Teichman

Butts

et al. 2020

American Journal of Health-System Pharmacy

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Purpose Although hyperglycemic crises can lead to a hypercoagulable state, few instances of associated mesenteric venous thrombosis (MVT) have been reported. Worsening abdominal pain in the context of shock requiring vasopressor support should prompt urgent further investigation. Summary A 44-year-old Hispanic male arrived at an emergency department with chief complaints of lethargy, polydipsia, and polyuria. His past medical history included type 2 diabetes, epilepsy, obesity, tobacco smoking, and noncompliance with his medications. On arrival the patient had a serum glucose concentration of >1,600 mg/dL, and hyperosmolar hyperglycemic syndrome (HHS) was diagnosed. The patient was admitted to the intensive care unit with respiratory failure and subsequently developed shock refractory to fluid resuscitation, necessitating vasopressor support. On hospital day 4, a computerized tomogram obtained for investigation of increasing abdominal tenderness revealed superior MVT and pneumatosis intestinalis. Despite an emergency laparotomy and enterectomy, the patient ultimately succumbed on hospital day 41 due to recurrent pneumonia complicated by acute respiratory distress syndrome and septic shock. Conclusion Shock that is refractory to aggressive fluid resuscitation, necessitating pressor support, in the setting of HHS or diabetic ketoacidosis should prompt investigation for the underlying source of shock. Other etiologies, including hypovolemic, cardiogenic, and obstructive shock, should be considered; however, infection is the leading trigger of hyperglycemic crises. Although rarely reported, MVT should be considered in the diagnostic algorithm in the absence of an identified infectious source. Prompt investigation should include use of diagnostic modalities such as computed tomography to assess for MVT.

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HHS – full or prophylactic anticoagulation?

Cited by 4 publications

References 8 publications

Controversies in the management of hyperglycaemic emergencies in adults with diabetes

Controversies in the management of hyperglycaemic emergencies in adults with diabetes

Management of Hyperosmolar Hyperglycaemic State (HHS) in Adults: An updated guideline from the Joint British Diabetes Societies (JBDS) for Inpatient Care Group

Mesenteric venous thrombosis: A lethal complication of hyperglycemic crises

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