Page 1403 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

976 PART 8: Renal and Metabolic Disorders

hyperosmolarity or acidosis. DKA can be graded based on the severity Delays in presentation to medical services and diagnosis have been
11
of acidosis (see below). However, other coexisting conditions at presen- recognized as contributing to mortality. Public education campaigns
26
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tation, which also affect the acid-base balance, may result in DKA being and frequent consultation with diabetes services have been shown to
graded incorrectly. Therefore, it is important to identify other factors reduce DKA rates in the pediatric population. 31,32
affecting the acid-base balance in patients at initial assessment and not
rely solely on pH and serum bicarbonate for risk stratification. Cerebral Edema: The pathophysiology of cerebral edema is uncertain.
13
It is an infrequent (0.3%-1%) complication in adult cases of DKA but
a major cause of mortality and morbidity in children. 29,33
With rising intracranial pressure and eventual brainstem hernia-
Mild pH 7.25-7.3 or serum bicarbonate 15-18 mEq/L tion, cerebral edema usual presents with headache and a gradual
Moderate pH 7.00-7.24 or serum bicarbonate 10-14 mEq/L deterioration in level of consciousness. Loss of sphincter tone, pupillary
changes, papilledema, and bradycardia may be followed by hyperten-
Severe pH <7.0 or serum bicarbonate <10 mEq/L
sion, seizures, and respiratory arrest.
The clinical picture should guide the diagnosis of cerebral edema.
Radiographic evidence of cerebral edema is relatively common in
The classical triad seen in DKA is hyperglycemia, ketosis, and a raised asymptomatic children with mild acidosis but can also be falsely reas-
anion gap metabolic acidosis. The key features of HHS are hypergly- suring as approximately 40% of children who develop cerebral edema
cemia, dehydration, and hyperosmolarity without significant ketosis. have no abnormality on initial imaging. 34,35 Neurological signs on pre-
Most patients can be readily separated into DKA or HHS, but there sentation, low partial pressure of arterial CO , use of sodium bicarbon-
2
can be overlap with clinical presentation. In HHS, plasma glucose can ate therapy, slowed rise in serum sodium during treatment, and higher
14
reach >60 mmol/L or 1080 mg/dL while it is unusual to have readings concentrations of serum urea are all associated with cerebral edema
>30 mmol/L or 541 mg/dL in DKA. Treatment regimens (see below) are in children. 36,37
similar but should be adjusted to suit individual patients. Dramatic fluxes in serum glucose, bicarbonate, sodium, and potas-
■ EPIDEMIOLOGY/INCIDENCE sium are seen in DKA during treatment. Rapid fluid resuscitation,
correction of glucose and electrolytes have all been postulated as
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The reported incidence of DKA in the Unites States has increased by precipitating or causative factors. Cerebral hypoperfusion and reper-
approximately 50% over the last 20 years. DKA was the primary rea- fusion injuries may play a role. The resultant cerebral ischemia and
39
son for admission for 81,000 hospital discharges in 1989. That figure hypoxia may generate inflammatory mediators. Other authors have
has risen steadily to 140,000 in 2009. Over the same period, hospital pointed to abnormalities in aquaporin channels and multiple metabolic
15
lengths of stay have fallen from 5.8 days to 3.4 days. In children with derangements. 40-42
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diabetes mellitus (aged <18 years) admitted to hospital, DKA represents The standard treatment regimen for those with cerebral edema is a
the primary reason for admission in 47% of discharges. 17,18 combination of intravenous manitol, 43,44 reduced IV fluid volume, con-
■ DIFFERENTIAL DIAGNOSIS in the intubated patient. Early recognition of those at risk and regular
sideration given to using hypertonic saline, and avoiding hypocapnea
45
33
Any cause of raised anion gap acidosis should be considered as an neurological surveillance are key.
alternative or a coexisting diagnosis in patients presenting with DKA. Gastroparesis: Acute hyperglycemia can result in gastroparesis. Typically
46
Ingestion of salicylates, ethylene glycol, sulfates, propylene glycol, and this resolves once patients become euglycemic but chronic hyperglycemia
47
methanol can result in a raised anion gap acidosis. Usually these can be can result in persistent gastric dysmotility. Enteric feeding may need
readily distinguished from DKA, as ketonemia is not present. Polyuria, to be suspended in the acute setting of a hyperglycemic crisis. The
polydipsia, dehydration, and hyperosmolarity are all features of diabetes presence of a succussion splash, persistent nausea, or vomiting should
insipidus but the absence of significant hyperglycemia at presentation prompt suspicion.
distinguishes it from HHS. DvT and Intra-Arterial Disease: Raised serum osmolality and viscosity in
Lactic acidosis and uremia can result in a similar biochemical profile hyperglycemic states can predispose to disseminated intravascular coagu-
to DKA but they can also complicate severe DKA/HHS. Their initial lation, intra-arterial and intravenous thrombus formation. 48,49 In vitro
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presence may worsen prognosis but rarely affects treatment regimen/ dysfunctional platelet and protein aggregation in patients with DM has
algorithm. Alcoholic and starvation ketosis rarely present with hypergly- been demonstrated in patients with poor glycemic control. 50-52 In the
cemia. Ketonemia and acidosis can be marked in alcoholic ketosis but absence of contraindications, thromboprophylaxis therapy should be
starvation ketosis rarely presents with significant acidosis. 20 commenced for patients with HHS. 53,54 Therapeutic doses of heparin
■ COMPLICATIONS should be reserved for those with a clinical evidence of an acute thrombus.
Death: Despite the exponential rise in incidence of new cases of Mucormycosis: Mucormycosis (previously known as zygomycosis) is a
diabetes, 21,22 there has been a fall in overall mortality for hyperglyce- fungal infection that can occur in immunocompromised patients and
mic crisis over the last 30 years. 23,24 Mortality remains high in elderly is an infrequent complication of hyperglycemic crisis. It can present
patients presenting with hyperglycemic crisis despite the significant with any combination of sinusitis, pyrexia, nasal discharge, headache,
improvements in survival rates. 14,24 Patients with HHS continue to facial/orbital edema, ophthalmoplegia, decreased visual acuity, or nasal
have a significantly higher mortality (10%-15%) than those with DKA ulceration. It carries a high mortality even when treated with appropri-
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(<3%). 25,26 This may be due to an older population with more comor- ate antifungal agents (amphotericin B). This opportunistic pathogen is
bidities. However, DKA is still the leading cause of death in children presumably carried in the nasal sinuses. Hyphae may invade the vascu-
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and young people (aged <24) with type 1 DM. 28,29 lature and structure surrounding the sinuses. Palatal necrosis, cerebral
Tackling these figures involves a combination of improving emer- involvement, and disseminated disease, all carry huge mortality risks.
gency care and preventative measures to reduce the frequency of delayed Early recognition and treatment are key. 56
presentation. Medical staff confronted with hyperglycemic emergencies Hypokalemia: Serum potassium often falls quickly during treatment.
should have local guidelines available to them and access to experienced The combination of intravenous insulin, saline without potassium
ICU and diabetes services. Recognition of gravely ill patients is vital as supplementation, and bicarbonate use contributes to dramatic
a low-dose insulin regimen in an ICU setting has been shown to signifi- changes in serum potassium. Frequent monitoring (initially 2 hourly)
cantly reduce DKA mortality. 30 is required to gauge the appropriate rate of replacement.

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