اشتباهات شایع در آی سی یو 16
Do not use Urine Output as a Measure of Volume Status in Patients who are Cold
Juan N. Pulido MD
Daniel R. Brown MD, PhD
Hypothermia is a clinical entity defined as a core body temperature less than 35Â° C (95Â° F) and is classified in four stages depending on the temperature, symptomatology, and impact on specific organ physiology (Table 171.1).
All organs are ultimately affected by hypothermia, including the kidneys. The renal response to cold is rapid and varies with the different stages of hypothermia. Initially, peripheral vasoconstriction results in relative central hypervolemia, producing an increase in urine output. This response, termed cold diuresis, has been described even in patients with mild to moderate hypothermia. The etiology of this phenomenon is multifactorial and includes an initial increase in cardiac output and renal blood flow due to hypothermia-induced changes in vascular capacitance. Other important contributors are nonosmotic suppression of antidiuretic-hormone (ADH) release by the hypothalamus and subsequent decreased renal tubular reabsorption. These responses usually begin as soon as the core body temperature reaches 35Â° C and become more pronounced until moderate hypothermia, when decreased renal blood flow and glomerular filtration rate (reduced 50% at 27Â° to 30Â° C) may lead to renal failure.
Watch Out For
Even in the setting of a large diuresis (the urine is usually dilute with osmolarity <300 mOsm/L and specific gravity <1.003), the kidneys are unable to handle nitrogenous waste due to tubular dysfunction. Although uncommon, electrolyte disturbances including hypernatremia, hyperchloremia, and hyperkalemia can occur and are more frequent as hypothermia progresses in duration and/or severity. Cold diuresis is exacerbated by ethanol ingestion and water submersion, which may coexist with hypothermia and can potentiate inappropriate diuresis by inhibiting ADH secretion.
It is important to understand the pathophysiology of this phenomenon when making clinical decisions regarding fluid management in hypothermic patients. The cold diuresis can be massive and generally creates a hypovolemic state that worsens with rewarming because
of the reverse changes in vascular tone as core body temperature is raised. If overlooked or underappreciated, this phenomenon can exacerbate electrolyte disturbances, contribute to hypotension, and result in prerenal stress.
Intravascular volume status should be closely monitored to avoid complications of this â€œphysiologically inappropriateâ€ renal response. Initially, it should be assumed that the patient is significantly dehydrated. Frequent measurements of electrolytes and hematocrit will help guide fluid therapy and electrolyte replacement and help monitor for dehydration. Central venous access should be considered to allow for safer electrolyte replacement and rapid volume administration, though electrolyte abnormalities may increase cardiac irritability and arrhythmia risk during catheter placement. Invasive arterial blood pressure monitoring should also be considered to facilitate laboratory determinations and to evaluate fluid responsiveness.
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