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Amboss: Dr. S. Majid, Presentation
Amboss: Dr. S. Majid, Presentation
Majid, Presentation
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CLINICAL SCIENCE
CLINICIAN
Hyperglycemic crises
Summary
Dr. S. Majid, Presentation
Acute hyperglycemia, or high blood glucose, may be either the initial presentation of diabetes
mellitus or a complication arising during the course of another disease.
Inadequate insulin replacement (e.g., noncompliance with treatment) or increased insulin demand
(e.g., during times of acute illness, surgery, or stress) may lead to acute hyperglycemia. In diabetic
ketoacidosis (DKA), which is more common in patients with type 1 diabetes, no insulin is available
to suppress lipolysis, resulting in ketone formation and acidosis. In a hyperosmolar hyperglycemic
state (HHS), which is more common in patients with type 2 diabetes, there is still
some insulin available and so there is minimal or no ketone formation. Clinical features of
both DKA and HHS include polyuria, polydipsia, nausea and vomiting, volume depletion (e.g., dry
oral mucosa, decreased skin turgor), and eventually mental status changes and coma. Features
unique to DKA include a fruity odor to the breath, hyperventilation, and abdominal pain. Patients
with HHS typically present with more extreme volume depletion than those with DKA. The mainstay
of treatment for both DKA and HHS consists primarily of IV fluid resuscitation, electrolyte repletion,
and insulin therapy.
Etiology
DKA, oftentimes precipitated by infection (e.g., pneumonia, urinary tract infection), is often
the initial manifestation of type 1 diabetes mellitus (∼ 30% of cases)!
References:[1]
Pathophysiology
Hypovolemia resulting from DKA can lead to acute kidney injury (AKI) due to decreased renal blood
flow! Hypovolemic shock may also develop.
DKA is an important cause of anion gap metabolic acidosis with respiratory compensation.
As a result of hyperglycemic hyperosmolality, potassium shifts along with water from inside
cells to the extracellular space and is lost in the urine.
Insulin normally promotes cellular potassium uptake but is absent in DKA, compounding
the problem.
A total body potassium deficit develops in the body, although serum potassium may be
normal or even paradoxically elevated.
Insulin deficiency → hyperosmolality → K+ shift out of cells + lack of insulin to
promote K+ uptake → intracellular K+depleted → total body K+ deficit despite normal or even
elevated serum K+
There is a total body potassium deficit in DKA. This becomes important during treatment,
when insulin replacement leads to rapid potassium uptake by depleted cells and patients may
require potassium replacement.
References:[1][2]
Clinical features
Polyuria, polydipsia + +
Dehydration + ++ (Profound)
Hyperventilation + -
Fruity breath + -
Known diabetics who present with nausea and vomiting should be immediately assessed
for DKA/HHS! Because patients with type 2 diabetes can still produce small amounts of insulin in
some cases, acute hyperglycemia progresses more slowly and serum glucose is significantly
elevated compared with patients with type 1 diabetes in DKA (> 600 mg/dL versus > 250 mg/dL).
References:[1][2][3][4]
Diagnostics
Approach [5][6]
Diagnostic workup to evaluate the underlying cause: HbA1c, CBC, ECG, infectious workup
BM Glucose < 600 mg/dL (< 33.3 mmol/L) > 600 mg/dL (> 33.3
P mmol/L)
About 10% of patients with DKA will be
euglycemic (e.g., glucose ≤ 250 mg/dL)
[5]
mmol/L)
Anion gap Elevated anion gap > 10 mEq/L (> 10 Normal anion gap <
mmol/L) 10 mEq/L (< 10
mmol/L)
DKA is the diagnosis in patients with type 1 diabetes who have hyperglycemia, ketonuria, and high
anion gap metabolic acidosis with decreased bicarbonate!
HHS is the diagnosis in patients with type 2 diabetes who have hyperglycemia and hyperosmolality!
Ketone levels should be ordered in all patients with high anion gap metabolic acidosis to evaluate
for euglycemic DKA.
Sodium:
Hyponatremia is common in both DKA and HHS, due to hypovolemic hyponatremia and
hypertonic hyponatremia
Always check corrected sodium for hyperglycemia.
Potassium in DKA: normal or elevated (despite a total body deficit)
Magnesium levels are typically low.
Phosphorus levels may be falsely elevated despite a total body deficit.
BUN and creatinine are often elevated. [9]
Dr. S. Majid, Presentation
HbA1c
Urine pregnancy test [11]
Serum transaminases
Abdominal ultrasound
Toxicology screen
Infection, myocardial infarction, and pancreatitis should be ruled out in all patients presenting with
a hyperglycemic crisis.
Management
Approach
IV access with two large-bore peripheral IV lines
Assess the severity of DKA.
Fluid resuscitation: initially with isotonic saline (0.9% NaCl), then 0.45% or 0.9% depending
on corrected serum sodium
Dr. S. Majid, Presentation
Initially treat DKA with normal saline and short-acting (regular) insulin.
First hour: isotonic saline solution (0.9% sodium chloride) at 15–20 mL/kg/hour (∼ 1000–
1500 mL bolus) [5][10][13]
Next 48 hours: Adjust IV fluid rate and composition according to CVP, urine output, blood
glucose, and corrected sodium levels.
Check corrected sodium for hyperglycemia.
If corrected serum sodium ≥ 135 mmol/L: 0.45% NaCl
If corrected serum sodium < 135 mmol/L: 0.9% NaCl
When serum glucose falls to < 200–250 mg/dL, add 5% dextrose to infusion.
Potassium
Potassium levels must be ≥ 3.3 mEq/L before insulin therapy is initiated
If potassium level is < 3.3 mEq/L, potassium should be repleted and rechecked prior to
giving any insulin.
If potassium level is < 5.3 mEq/L, the patient will likely require potassium
repletion once insulin therapy is started
Maintain serum potassium between 4–5 mEq/L.
Serum K +
Recommended dose [14]
It is critical that potassium levels are confirmed to be > 3.3 mEq/L before administering insulin,
as insulin will lower serum potassium and potentially cause severe hypokalemia.
Insulin [5][13][15]
The goal is to decrease blood glucose levels by 10% per hour (∼50–75 mg/dL/hour).
Treatment with subcutaneous rapid-acting insulin analogues on a regular medical ward may
be considered in cases of mild DKA.
Acidosis usually resolves with fluids and insulin therapy and the use of IV bicarbonate is
usually not necessary
If pH < 6.9 despite adequate IV fluid resuscitation, administer IV sodium bicarbonate.
Monitoring of volume status, serum glucose, serum electrolytes, and acid-base status at regular
intervals is essential.
DKA HHS
Glucose < 200 mg/dL Normalization of serum osmolality (i.e., < 320
PLUS at least two of the mOsm/kg)
following: Normal mental status
Venous pH > 7.30
Serum bicarbonate ≥ 15 mEq/L
Anion gap ≤ 12 mEq/L
ABCDE survey
Confirm diagnosis with blood gas, BMP, serum osmolality, serum ketones,
and urine ketones.
Start continuous insulin IV infusion with hourly POC glucose checks once serum
potassium is confirmed > 3.3 mEq/L.
Adjust fluid resuscitation based on corrected sodium for hyperglycemia, serum glucose,
and clinical response.
Identify and treat the underlying cause (e.g., medication noncompliance, infection).
Order monitoring labs (e.g., BMP, serum osmolality, and blood gas every 2–4 hours).
Differential diagnoses
All etiologies of altered mental status must be considered in the differential diagnosis of DKA/HHS!
Intoxication and other endocrine disorders, as well as gastroenteritis, myocardial
infarction, pancreatitis, and other causes of high anion gap metabolic acidosis, should all be
excluded.
DKA/HHS Hypoglycemia
Muscle ↓↓ ↑↑ (tremor)
tone
DKA/HHS Hypoglycemia
Complications
Sources
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