Obese Children: Challenges in the ICU
Meaghan Mungekar, MD*
Pediatric Hospitalist
Beth Israel Medical Center
New York, New York, USA
Edward E. Conway Jr., MD, MS, FCCM**
Chairman, Department of Pediatrics
Chief, Pediatric Critical Care Medicine
Beth Israel Medical Center
New York, New York, USA
The prevalence of childhood obesity is increasing worldwide. Recent studies estimate that 16.5% of children in the United States between the ages of 6 and 19 are overweight (body mass index [BMI] 85th to 94th percentile for age and gender) and 17.1% are obese (BMI ≥ 95th percentile for age and gender).(1) As the proportion of obese children in the general population increases, it is likely that more children requiring intensive care will be obese. Studies of obese adults in critical care units have revealed poorer outcomes and increased mortality(2); however, similar studies on children are lacking. Insulin resistance, hypercoagulability and inflammation characterize obesity as a disease process that mimics critical illness.(3) Obesity is a chronic inflammatory state that diminishes immune and metabolic reserves. An increased BMI requires increased cardiovascular, respiratory and metabolic work, resulting in a markedly diminished physiologic reserve. The practitioner in the pediatric intensive care unit (PICU) should be familiar with some of the basic physiologic derangements that may be seen in these patients.
The metabolic syndrome describes a cluster of cardiovascular risk factors, including hypertension, dyslipidemia, insulin resistance and central adiposity.(4) Approximately one-third of obese adolescents have metabolic syndrome, compared to 7% of overweight adolescents and 0.6% of adolescents with normal BMI.(5) Adipose tissue releases inflammatory, thrombotic and vasoactive mediators, contributing to the development of the metabolic syndrome and leading to childhood atherosclerosis and a markedly increased risk of cardiovascular disease in adulthood.(6) Obesity is an independent risk factor for hypertension in children and adolescents,(7-10) and is currently defined as systolic blood pressure and/or diastolic blood pressure ≥95th percentile for gender, age and height on three separate occasions.(11) Obese children and adolescents have impaired endothelial and smooth muscle function,(9) as well as decreased parasympathetic nervous system activity,(12) which leads to reduced dilation of peripheral arteries. Increased left ventricular mass has been found in both prepubertal and pubertal obese children, an effect seen regardless of blood pressure classification.(10) This evidence of early end-organ damage can help to guide decisions on the use of antihypertensive medication. Severe, uncontrolled hypertension in children may cause neurological sequelae such as seizures, encephalopathy or stroke, as well as congestive heart failure.(11) Critically ill obese children should have their blood pressure closely monitored using appropriately sized cuffs that cover two-thirds the length of the upper arm with the bladder length encompassing the entire arm circumference.(9)
Childhood obesity is associated with impaired glucose tolerance and insulin resistance, which manifests externally as acanthosis nigricans.(4) Insulin resistance, in turn, is associated with lipid abnormalities, inflammatory markers, elevated blood pressure, and left ventricular hypertrophy.(6) Stressinduced hyperglycemia is often seen in critically ill patients(13) and may be more pronounced in children with impaired glucose tolerance at baseline. The release of catecholamines, cortisol, glucagon, and proinflammatory mediators leads to a state of insulin resistance and hyperglycemia.(13) Although this initially may be advantageous (providing more energy to organs and tissues with increased demand), prolonged hyperglycemia can lead to free radical formation, cellular damage and impaired immunity – ultimately resulting in poorer outcomes and increased mortality.(13,14) Although there is a paucity of data on the relationship between glucose control in critically ill children and outcomes, evidence from the adult literature suggests that strict glucose control in intensive care units improves both morbidity and mortality.(14)
A subset of children with impaired glucose tolerance will progress to develop type 2 diabetes,(4) which comprises 8% to 45% of newly diagnosed cases of diabetes in children.(6) The rise in type 2 diabetes seems to parallel the increase in childhood obesity.(12) The symptoms of type 2 diabetes are often subtle, which may lead to a delay in diagnosis. Children can present with hyperglycemic hyperosmolar syndrome (HHS), an entity that carries significant morbidity and mortality. HHS is characterized by hyperglycemia (blood glucose >600 mg/dL) and elevated serum osmolality (>320 mmol/kg) with mild metabolic acidosis and no ketosis. With the slower onset of symptoms, these patients can lose 15% to 20% of total body water, leading to severe hypovolemia; therefore, they require aggressive fluid resuscitation. The adult mortality rate for HHS is 10% to 15%; the rate in children is unknown, although case reports have shown poor outcomes, including rhabdomyolysis, multiorgan failure and death.(12)
Asthma has increased in prevalence in tandem with the rise in childhood obesity.(15,16) Elevated BMI is associated with higher rates of asthma and wheezing.(16,17) Leptin, a hormone produced by adipose cells, is known to have a positive correlation with both BMI and asthma,18 possibly due to the pro-inflammatory effects of leptin(18) as well as its association with hypoventilation in obese individuals.(19) In addition, obesity results in a restrictive lung pattern due to both increased pulmonary blood volume and increased chest wall mass from adipose tissue. Obese children with asthma miss more school days, require more medications, and have lower peak flow rates than nonobese asthmatics.(17) In the PICU, obese children admitted for status asthmaticus have increased lengths of stay and longer courses of intensive therapy, including the need for supplemental oxygen and administration of continuous beta-agonists and intravenous steroids.(15)
Obesity is a risk factor for the development of obstructive sleep apnea (OSA) and correlates with more severe symptoms.(20-23) Approximately 37% to 46% of obese children have OSA.(21) Weight loss decreases both upper airway obstruction and OSA symptoms.(20) Obese children with OSA who undergo tonsillectomies and adenoidectomies have more intraoperative respiratory complications, including the need for multiple intubation attempts and post-induction desaturations. In addition, they are more likely to be hospitalized postoperatively and have a longer length of stay.(22) Postoperative upper airway obstruction in these obese patients may be caused by excess neck tissue compressing the airway, hypoventilation due to decreased chest wall compliance and upward displacement of the diaphragm secondary to abdominal obesity, and decreased airway tone after anesthesia.(21) Postobstructive pulmonary edema is a known complication following tonsillectomy and adenoidectomy; it is unknown whether there is an increased incidence in obese patients.(21) Preoperative polysomnography is recommended for all obese patients to determine OSA severity, which can guide the need for intensive care monitoring postoperatively.(21-23) If left untreated, OSA can lead to pulmonary hypertension and cor pulmonale caused by chronic nocturnal hypoxemia.(20)
In general, obese children undergoing surgical procedures are at increased risk for complications.(24,25) They have significantly higher American Society of Anesthesiology (ASA) scores, given their medical comorbidities.(25) Vascular access can be difficult to obtain and control of the airway is challenging.(24) Medications, especially sedatives and narcotics, should be given in dosages based on ideal body weight.(24,26) Postoperatively, there is an increased risk of upper airway obstruction and desaturations.(24,25) Obesity is an independent risk factor for deep venous thrombosis; therefore, postoperative obese patients in particular should receive appropriate prophylaxis.(26) A discussion of bariatric surgery (gastric bypass and laparoscopic banding) is beyond the scope of this paper; however, these procedures should be considered only in extreme cases and performed by a well-trained team of pediatric specialists.(27)
As the prevalence of childhood obesity increases, conditions once considered to be only “adult” diseases will continue to manifest in children and adolescents. Awareness of these comorbidities allows care providers to anticipate potential complications in critically ill obese children. More research is needed to understand better the effect of obesity on outcomes in the PICU and to determine strategies to improve morbidity and mortality for these patients.
References:
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Disclosures:
*Author has no disclosures to report
**Author has no disclosures to report
