Page 1404 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 101: Hyperglycemic Crisis and Hypoglycemia 977

Dysglycemia: Iatrogenic hypoglycemia is a common occurrence during measurements), and 2 hourly electrolyte profiles should be performed.
the course of treatment of hyperglycemia. Frequent blood glucose It is extremely helpful to have charts prepared to monitor these variables
monitoring and using low-dose insulin therapy lessen the risk of this in graphical format either by hand or in the electronic medical record.
complication. Rebound hyperglycemia and ketosis may arise from
either inappropriate overlap of intravenous with subcutaneous insulin Potassium: HHS and DKA often result in a 3 to 5 mEq/L total body
or failure to continue insulin therapy long enough. Twenty-four to potassium deficit. +
48 hours of IV therapy may be needed to completely “turn off” ketone- IV insulin therapy promotes an intracellular shift of K through the
+
+
+
generating enzymes in the liver. glucose Na /K transporter. Large volumes of IV saline without K supple-
mentation can further lower serum K . Concomitant hypomagnesemia
+
Other Complications: Rhabdomyolysis is a rare but potentially fatal can exacerbate hypokalemia through increased renal K loss. Untreated
59
+
finding in hyperglycemic crisis. Serum creatine kinase measurement hypomagnesemia can render hypokalemia refractory to treatment with
26
should be performed on all patients presenting with HHS. Acute lung potassium supplementation. Careful monitoring and supplementation of
injury is also an established complication. Changes in alveolar capil- K is required. If patients are hypokalemic on presentation, potassium can
+
lary permeability coupled with overzealous fluid resuscitation may be given along with IV insulin. 60
result in noncardiogenic pulmonary edema. 57 Phosphate: Profound hypophosphatemia is associated with muscle
■ MANAGEMENT weakness (cardiac and skeletal), hemolysis, and rhabdomyolysis.
HHS and DKA are medical emergencies and should be managed in a Hypophosphatemia as a consequence of hyperglycemic crisis is relative
common, usually mild and self-limiting. Phosphate supplementation
unit with during DKA has not shown any significant clinical benefit. Indeed
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• Experienced nursing and medical staff, trained in the management phosphate therapy during DKA has been associated with hypocal-
62
of hyperglycemic emergencies cemia and hypomagnesemia. Therapy with IV phosphate should
• Regularly updated guidelines for DKA and HHS treatment therefore be reserved for patients with profound (<0.32 mmol/L or
1 mg/dL) hypomagnesemia, rhabdomyolysis, or hemolytic anemia.
• Access to frequent and timely biochemical investigations
Bicarbonate: Many international and local guidelines have incorporated
Goals of Therapy intravenous bicarbonate use to correct profound diabetic ketoacidosis in
63
• Restoration of circulatory volume and improved tissue perfusion adults. Alkalization is felt to improve myocardial contractility. However,
bicarbonate use may lower serum potassium and ionized calcium levels
• Steady reduction of serum glucose and osmolality/ketonemia and decrease peripheral tissue oxygenation by increasing the affinity
• Correction of electrolyte imbalances between hemoglobin and oxygen. There are few randomized control
64
65
• Identification and treatment of precipitant factors trials to assess any clinical benefits. Its use remains contentious.
Bicarbonate use in children and adolescence is not recommended and
• Identification and treatment of potential complications there is evidence to suggest it may worsen cerebral edema and cause a
There are multiple local and international guidelines available. 13,58 paradoxical drop in the pH of cerebrospinal fluid. 33,66
The key principles of treatment will be outlined here. Local guidelines/ Predisposing Factors: Insulin omission and new presentation with DM
protocols should be available and adhered to. However, the ability for (usually type 1 DM but also type 2 DM and in rare cases of MODY)
senior medical staff to individualize therapy and modify guidelines in represent a large portion of the cases of hyperglycemic crisis, but
the patient with a complex presentation is also important.
other potential factors should be sought and treated. Some of the
67
Fluids: In both HHS and DKA, patients are volume deplete varying more common predisposing factors are listed in Table 101-3.
from 6 to 10 L. Infectious precipitants often arise from pelvic inflammatory disease,
The choice of intravenous fluid and rate of infusion is dictated by meningitis, or sources in the skin, sinuses, or respiratory and urinary
68
the serum osmolality and patient hydration status. Typically 0.45% tracts. The neutrophil and total white cell counts are often raised in
11
saline is used in adults with HHS or hypernatremia patients with DKA. hyperglycemic crisis. The etiology is uncertain but leukocytosis may
Otherwise isotonic saline (0.9%) is used. Regular monitoring of the be in part due to elevated cortisol, catecholamines, and proinflammatory
69
patients volume status is necessary as most guidelines suggest a high rate cytokines. Given the high incidence of coexisting infection and high
of fluid replacement. Five percent dextrose should be added to the fluid mortality associated with HHS, there should be low threshold for early
regimen once plasma glucose falls below 250 mg/dL. broad-spectrum antibiotic use.
Fluid replacement should be guided by bedside ultrasound or other
dynamic predictors of fluid-responsiveness (see Chap. 34). Intensive
monitoring may be useful in the first 24 to 48 hours in patients with TABLE 101-3 Predisposing Factors for Hyperglycemic Crisis
HHS/DKA with coexisting congestive cardiac failure, sepsis, or renal New presentation of DM
failure. Pancreatitis
Insulin and Glucose Monitoring: Continuous insulin therapy is particu- Acute major illness 68
larly important in DKA as the half-life of IV insulin is short and ketosis Sepsis and infection
can recur quickly. DKA itself is an insulin-resistant state and rela- Dehydration 67
tively high doses are often needed in the initial period. A 0.1 unit/kg Insulin omission
bolus followed by a 0.1 unit/kg/h infusion is a reasonable starting Poor compliance 86 87
point in DKA. In HHS, blood glucose can drop dramatically with CSII pump failure
rehydration alone and lower doses of insulin are required. Medications/drugs
88
Regular glucose monitoring is needed as insulin sensitivity changes Cocaine
markedly in the first 24 hours of therapy. When glucose falls below Atypical antipsychotics 89
250 mg/dL, intravenous fluids should include 5% dextrose and the IV Glucocorticoids
insulin therapy continued. Hourly urine output, hourly glucose mea- High dose thiazide diuretics
surement, heart rate, blood pressure, venous pH (2-4 hourly, rarely are Sympathomimetic, eg, dobutamine
repeated arterial blood gas measurements required purely for pH/HCO Alcohol
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