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Understanding Hyperglycemic Crises

Hyperglycemic crises like diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are acute complications of diabetes characterized by uncontrolled hyperglycemia. DKA involves a triad of hyperglycemia, metabolic acidosis, and ketosis and can develop quickly over 24 hours. HHS involves severe hyperglycemia, dehydration, and hyperosmolality without significant ketosis and develops over days to weeks. Precipitating factors include infection, discontinuing insulin, medical issues, drugs, and psychological problems. Treatment involves fluid therapy, insulin, potassium supplementation, and bicarbonate as needed followed by transition to subcutaneous insulin. Complications can include hyp

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0% found this document useful (0 votes)
73 views13 pages

Understanding Hyperglycemic Crises

Hyperglycemic crises like diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS) are acute complications of diabetes characterized by uncontrolled hyperglycemia. DKA involves a triad of hyperglycemia, metabolic acidosis, and ketosis and can develop quickly over 24 hours. HHS involves severe hyperglycemia, dehydration, and hyperosmolality without significant ketosis and develops over days to weeks. Precipitating factors include infection, discontinuing insulin, medical issues, drugs, and psychological problems. Treatment involves fluid therapy, insulin, potassium supplementation, and bicarbonate as needed followed by transition to subcutaneous insulin. Complications can include hyp

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phyna27
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PPTX, PDF, TXT or read online on Scribd

Hyperglycemic

Crises
Source : American Diabetes
Association
Introduction

• Hyperglicemic crises, including diabetic


ketoacidosis (DKA) and the hyperosmolar
hyperglycemic state (HHS) are the two most serious
acute metabolic complications of diabetes.
• DKA is characterized by the triad of
uncontrolled hyperglycemia, metabolic acidosis,
and increased total body ketone concentration.

• HHS is characterized by severe hyperglycemia,


hyperosmolality, and dehydration in the absence
of significant ketoacidosis.
Patho
genesis
Precipitating Factors
• Infection
• Discontinuation of or inadequate insulin therapy
• Cerebrovascular accident
• Myocardial infarction
• Psychological problems and eating disorder
• Drugs
• corticosteroids, thiazides, sympathomimetic agents,
pentamidine, and atypical antipsychotic
Diagnosis
DKA HHS
evolves within a short time frame (typically evolves over several days to weeks.
24 h).
• History
classical and
clinical physical
picture includesexamination
a history of polyuria, polydipsia, weight loss, vomiting,
dehydration, weakness, and mental status change
poor skin turgor, Kussmaul respirations (in DKA), tachycardia, and hypotension
Focal neurologic signs (hemianopia and
hemiparesis) and seizures (focal or
generalized)
Nausea, vomiting, diffuse abdominal pain
are frequent in patients with DKA
Laboratory Findings
Differential Diagnosis
• Starvation ketosis and alcoholic ketoacidosis;
• distinguished by clinical history and by plasma glucose
concentrations that range from mildly elevated (rarely 200
mg/dl) to hypoglycemia.

• Lactic acidosis;
• Ingestion of drugs
• such as salicylate, methanol, ethylene glycol, and paraldehyde;

• Acute chronic renal failure


Treatment

• Fluid therapy
• Insulin therapy
• Potassium
• Bicarbonate therapy
• Transition to subcutaneous insulin
Complications

• Hypoglycemia and hypokalemia are two


common complications.
• Cerebral edema
• Commonly in children, rarely in adults.
Prevention
1. Early contact with the health care provider.
2. Emphasizing the importance of insulin never to
discontinue without contacting the health care team.
3. Review of blood glucose goals.
4. Having medications available to suppress a fever and
treat an infection.
5. Initiation of an easily digestible liquid diet containing
carbohydrates and salt when nauseated.

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