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978 PART 8: Renal and Metabolic Disorders

In many cases, the precipitating factor for the hyperglycemia is clear. In spontaneous hypoglycemia, the goal is identification of the etiology
Despite this, chest radiograph, blood and urine cultures are almost and treatment. Hypoglycemic disorders are rare aside from critically ill
always indicated following the initial clinical assessment and initiation patients or those with an obvious drug cause.
of therapy. More than one etiology or a second infection as a complica- ■
tion is possible. There should be a low threshold for treating acutely SYMPTOMS AND SIGNS
unwell patients with antimicrobials while awaiting the formal culture Symptoms of hypoglycemia are nonspecific but typically are divided into
results. CSF glucose results need to be interpreted with caution in neuroglycopenic symptoms and those affecting the autonomic nervous
patients with hyperglycemia. 70 system (see Table 101-4). Given the array of potential and variable symp-
Amylase and lipase may be raised in patients with DKA without toms, it can be difficult to ensure hypoglycemia is the cause. Patients who
active pancreatitis. However, acute pancreatitis is an established cause are not on treatment to lower blood glucose must satisfy Whipple triad in
of DKA. Some authors suggest a lipase of >400 U in those with a order to attribute their symptoms/signs to a hypoglycemic disorder.
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combination of DKA and abdominal pain as this is highly suggestive of
underlying abdominal pathology. 72 Whipple Triad
Deep venous and pulmonary embolic disease along with coronary a) Symptoms in keeping with hypoglycemia (Table 101-4)
and cerebrovascular intra-arterial thrombosis can precipitate or compli-
cate HHS. In the absence of a bleeding disorder or active GI bleed, pro- b) Low plasma glucose at time of symptoms
26
phylaxis with low-molecular-weight heparin is suggested. Therapeutic c) Resolution of symptoms following treatment and elevation of plasma
doses should be reserved for those patients with overt signs suggestive glucose
of an acute thromboembolism. Glucose meters lose accuracy at lower serum glucose concentrations
Patients with chronic kidney disease and hyperglycemia represent a <70 mg/dL (3.9 mmol/L) and are not used for the diagnosis of hypogly-
particularly challenging group. Anuric patients without osmotic diuresis cemic disorders. 79,80
sequester free water from the intracellular compartment. They may have
signs and symptoms of congestive cardiac failure rather than the volume ■ CAUSES
depletion usually evident in HSS. IV insulin without IV hydration is
the treatment of choice. Restoration of euglycemia causes free water to Insulin, sulfonylurea, and alcohol use are responsible in the majority of
73
shift back to the intracellular compartment from the intravascular space. cases in adults. Combinations of DDP4 inhibitors or incretin agonists
Continuous venovenous hemofiltration dialysis (CVVHD) may also be with sulfonylureas can increase the incidence of hypoglycemic events.
required to treat refractory metabolic acidosis since ketoacids may persist. 74 Over 150 other drugs have been implicated, but the majority of these
have very low-quality data to substantiate the association. Some of
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Transitioning: Patients already on insulin therapy may be transitioned the causes seen in adults are listed in Table 101-5. The physiological
back to their regular doses with resolution of DKA. Resolution is response to hypoglycemia is a dynamic process with varying thresholds
determined by pH >7.3, HCO >18, and glucose <200 mg/dL. in individuals that can change significantly over time (Table 101-6). 78,82,83
−
3
Ketonuria can persist for a number of days post–DKA, but ketonemia Understanding of the normal response to falling blood glucose can aid
can be more accurately assessed using serum β-hydroxybutyrate and in the identification of the pathophysiological mechanism commonly
monitoring the anion gap (Table 101-1). responsible for hypoglycemia. These include
Sudden withdrawal of IV insulin can result in dramatic rebound hyper-
glycemia. An overlap of 1 to 4 hours between IV and subcutaneous basal a) Inappropriate insulin secretion or administration (eg, sulfonylurea or
exogenous insulin use)
insulin is recommended depending on the subcutaneous insulin used.
The slower onset the insulin, the longer the overlap must be. Not giving a b) Insufficient counterregulatory hormone(s)
sufficient overlap of insulins remains a common error in the ICU setting. c) Increased metabolic demands
Patients previously untreated with insulin are often commenced on a d) Reduced availability of glycogen
basal bolus regimen initially. Patients with type 1 DM typically require a
total daily dose of 0.5 to 1.0 unit/kg/day. The IV insulin requirements can e) Reduced sensation/awareness of symptoms
75
also be used as a guide to estimating subcutaneous insulin doses. Frequently Neonates and infants have a lower reference range for euglycemia,
the insulin requirements fall over the subsequent few days postepisode. varying symptomatology, and a different list of causes of hypoglycemia.
It is difficult to assign a set numerical cutoff for hypoglycemia in this
HYPOGLYCEMIA population. Differing gestational age, postnatal age, level of ketonemia,
and concomitant illness can all affect glycolysis, making patient-specific
plasma glucose ranges problematic. Infants also have nonspecific signs
KEY POINTS of hypoglycemia (poor feeding, jitteriness, hypotonia, seizures, brady-
• Most commonly seen in patients treated for DM. cardia, etc). The American Academy of Pediatrics has tried to address
the difficulties with diagnosing and treating hypoglycemia in the infant/
• Insulinoma is a rare cause of hypoglycemia.
newborn with recently published guidelines. 84
• Oral treatment with rapid acting carbohydrate is the preferred
treatment.
TABLE 101-4 Signs and Symptoms of Hypoglycemia
INTRODUCTION Neuroglycopenic Autonomic
Typically iatrogenic causes of hypoglycemia are seen in patients with Irritability Tremor
known DM or on medication with the known side effect of hypoglyce- Confusion Tachycardia
mia. Symptomatic hypoglycemia on average affects patients with type 1 Psychomotor dysfunction Palpitations
DM twice a week, and, remarkably, 2% to 4% of patients with type 1 DM
will die as a result of hypoglycemia. 76,77 Rapid elevation of glucose and Behavioral changes Anxiety
modification of therapy to reduce the risk of significant hypoglycemia are Focal neurological deficit Hunger
the primary goals in patients with iatrogenic hypoglycemia. There may be Coma Diaphoresis
absence or blunting of symptoms in patients with long-standing diabetes
or those exposed to persistent or frequent episodes of hypoglycemia. 78 Seizure Paresthesia

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