Julin F. Tang

Dexmedetomidine controls agitation and facilitates reliable, serial neurological examinations in a non-intubated patient with traumatic brain injury.

IntroductionWe report the effective use of dexmedetomidine in the treatment of a patient with a history of chronic alcohol abuse and an acute traumatic brain injury who developed agitation that was unresolved if from traumatic brain injury, or alcohol withdrawal or the combination of both. Treatment with benzodiazepines failed; lorazepam therapy obscured our ability to do reliable neurological testing to follow his brain injury and nearly resulted in intubation of the patient secondary to respiratory suppression. Upon admission to hospital, the patient was first treated with intermittent, prophylactic doses of lorazepam for potential alcohol withdrawal based upon our institution’s standard of care. His neurological examinations including a motor score of 6 (obeying commands) on his Glasgow Coma Scale testing, laboratory studies, and repeat CT head imaging remained stable. For lack of published literature in diagnosing symptoms of patients with a history of both alcohol withdrawal and traumatic brain injury, a diagnosis of agitation secondary to presumed alcohol withdrawal was made when the patient developed acute onset of tachycardia, confusion, and extreme anxiety with tremor and attempts to climb out of bed requiring him to be restrained. Additional lorazepam doses were administered following a hospital-approved protocol for titration of benzodiazepine therapy for alcohol withdrawal. The patient’s mental status and respiratory function deteriorated with the frequent lorazepam dosing needed to control his agitation. Dexmedetomidine IV infusion at a rate of 0.5 mcg/kg/h was then administered and was titrated ultimately to 1.5 mcg/kg/h. After 8 days of therapy with dexmedetomidine, the patient was transferred from the ICU to a step-down unit with an intact neurological examination and no evidence of alcohol withdrawal. Airway intubation was avoided during the patient’s entire hospitalization. This case report highlights the intricate balance between the side effects of benzodiazepine sedation for treatment of agitation and the difficulties of monitoring the neurological status of non-intubated patients with traumatic brain injuryConclusionGiven the large numbers of alcohol-dependent patients who suffer a traumatic brain injury and subsequently develop agitation and alcohol withdrawal in hospital, dexmedetomidine offers a novel strategy to facilitate sedation without neurological or respiratory depression. As this case report demonstrates, dexmedetomidine is an emerging treatment option for agitation in patients who require reliable, serial neurological testing to monitor the course of their traumatic brain injury.

Calculation of Physiologic Dead Space: Comparison of Ventilator Volumetric Capnography to Measurements by Metabolic Analyzer and Volumetric CO2 Monitor

BACKGROUND: Calculation of physiologic dead space (dead space divided by tidal volume [VD/VT]) using the Enghoff modification of the Bohr equation requires measurement of the partial pressure of mean expired CO2 (PĒCO2) by exhaled gas collection and analysis, use of a metabolic analyzer, or use of a volumetric CO2 monitor. The Dräger XL ventilator is equipped with integrated volumetric CO2 monitoring and calculates minute CO2 production (V̄CO2). We calculated PĒCO2 and VD/VT from ventilator derived volumetric CO2 measurements of V̄CO2 and compared them to metabolic analyzer and volumetric CO2 monitor measurements. METHODS: A total of 67 measurements in 36 subjects recovering from acute lung injury or ARDS were compared. Thirty-one ventilator derived measurements were compared to measurements using 3 different metabolic analyzers, and 36 ventilator derived measurements were compared to measurements from a volumetric CO2 monitor. RESULTS: There was a strong agreement between ventilator derived measurements and metabolic analyzer or volumetric CO2 monitor measurements of PĒCO2 and VD/VT. The correlations, bias, and precision between the ventilator and metabolic analyzer measurements for PĒCO2 were r = 0.97, r2 = 0.93 (P < .001), bias −1.04 mm Hg, and precision ± 1.47 mm Hg. For VD/VT the correlations were r = 0.95 and r2 = 0.91 (P < .001), and the bias and precision were 0.02 ± 0.04. The correlations between the ventilator and the volumetric CO2 monitor for PĒCO2 were r = 0.96 and r2 = 0.92 (P < .001), and the bias and precision were −0.19 ± 1.58 mm Hg. The correlations between the ventilator and the volumetric CO2 monitor for VD/VT were r = 0.97 and r2 = 0.95 (P < .001), and the bias and precision were 0.01 ± 0.03. CONCLUSIONS: PĒCO2, and therefore VD/VT, can be accurately calculated directly from the Dräger XL ventilator volumetric capnography measurements without use of a metabolic analyzer or volumetric CO2 monitor.

Management of acidosis during lung-protective ventilation in acute respiratory distress syndrome.

In ARDS, when acidosis complicates LPV, the goal of alkali therapy is to maintain arterial pH at a safe level (> or = 7.20). A pure respiratory acidosis generally does not require alkali therapy. If the Pplat is greater than 30 cm H2O, and the respiratory rate equals the upper limit (35-40 breaths/minute), then V(E) is slowly titrated down by approximately 1 L/hour, so that PaCO2 increases by 10 mm Hg/hour or less. Alkali therapy is indicated for either a metabolic acidosis or a mixed acidosis. The choice of buffer is based on the type of acidosis, cardiorespiratory status, and lung mechanics. Slow infusions of NaHCO3 can be used to treat non-anion gap metabolic acidosis and some forms of increased anion gap acidosis. Using NaHCO3 to treat type A (hypoxia-related) lactic acidosis can be hazardous, particularly under conditions of hypoxemia, inadequate circulation, and limited alveolar ventilation. Under these circumstances, THAM is the preferable buffer because it does not increase PaCO2 and is excreted by the kidneys. When renal failure is present, CRRT is indicated to manage acidosis. When ARDS is complicated by traumatic or hemorrhagic shock, overresuscitation with Cl(-)-rich solutions should be avoided to prevent metabolic acidosis.

Physiologic response of human brain death and the use of vasopressin for successful organ transplantation

The dynamic physiologic response of human brain death and the impact of vasopressin on successful organ transplantation is reported. A 60-year-old woman was admitted to the intensive care unit after severe traumatic brain injury resulting in brain death. Initial Cushing reflex was followed by a precipitous decrease in systemic blood pressure that was refractory to the alpha-agonist phenylephrine. After intravenous vasopressin was given, hemodynamic stability was restored and maintained until successful organ transplantation. Vasopressin, a catecholamine-sparing vasopressor and antidiuretic agent, may be an effective agent in the treatment of refractory hypotension after brain death prior to organ transplantation.

A Case of Unrecognized Intrathoracic Placement of a Subclavian Central Venous Catheter in a Patient with Large Traumatic Hemothorax.

Traditional recommendations suggest placement of a subclavian central venous catheter (CVC) ipsilateral to a known pneumothorax to minimize risk of bilateral pneumothorax. We present the case of a 65-year-old male with a right hemopneumothorax who was found to have intrathoracic placement of his right subclavian CVC at thoracotomy despite successful aspiration of blood and transduction of central venous pressure (CVP). We thus recommend extreme caution with the interpretation of CVC placement by blood aspiration and CVP measurement alone in patients with large volume ipsilateral hemothorax.