Transient Diabetes Insipidus After Discontinuation of Vasopressin in Neurological Intensive Care Unit Patients: Case Series and Literature Review.

BACKGROUND: Arginine vasopressin (AVP) is a common second-line or third-line vasopressor used in critically ill neurosurgical patients. Neurosurgical indications include hyperdynamic therapy for vasospasm, maintenance of cerebral perfusion pressure in patients with intracranial hypertension, and prevention of hypotension in patients with sepsis. CASE DESCRIPTION: A series of 6 neurosurgical patients receiving AVP infusions developed severe but transient diabetes insipidus (tDI) after cessation of AVP. To our knowledge, no previous reports of this phenomenon in neurosurgical patients have been published. We reviewed the clinical histories, intensive care unit treatment, medication administration records, and laboratory values of these patients, and we found recurrent elevated serum sodium and urine output and decreased urine specific gravity after discontinuation of AVP. Resolution of tDI occurred upon resumption of AVP or administration of desmopressin. Elevated serum sodium levels were often severe, resulting in worsened clinical outcomes. When AVP was resumed, tDI typically recurred if AVP was again tapered and discontinued. Routine administration of desmopressin was useful in controlling sodium levels until the tDI resolved. CONCLUSIONS: Recognition of this phenomenon has caused us to change our clinical management of neurosurgical patients receiving AVP. We hypothesize that tDI is caused by downregulation of the V2 receptor mass in the renal distal convoluted tubule and collecting duct cells. When AVP is discontinued, patients develop nephrogenic tDI secondary to decreased V2 receptor binding, which explains why desmopressin is effective in correcting tDI. Future research includes a large prospective study to determine risk factors for tDI, its incidence, and its pathophysiology.

Rare Variants in Cardiomyopathy Genes Associated With Stress-Induced Cardiomyopathy.

BACKGROUND: Stress-induced cardiomyopathy (SIC) is a poorly understood condition associated with periods of emotional and physical stress. The clinical approaches for management of SIC are supportive and reactive to patient symptoms. OBJECTIVE: To utilize next-generation exome sequencing to define genetic variation associated with, and potentially responsible for, this disease. METHODS: We performed exome sequencing of 7 white female patients with SIC. Filtering of the identified variants was performed to limit our investigation to those sequences that passed quality control criteria, were rare or novel, were determined algorithmically to have high impact on the associated protein, and were within regions of high species conservation. All variants were verified by using Sanger sequencing. RESULTS: Exome-sequencing analysis revealed that each patient carried predicted deleterious variants affecting known cardiomyopathy genes. In each case, the identified variant was either not previously found in public human genome data or was previously annotated in a database of clinical variants associated with cardiac dysfunction. CONCLUSION: Patients with SIC harbor deleterious mutations in established cardiomyopathy genes at a level higher than healthy controls. We hypothesize that patients at highest risk for SIC likely live in a compensated state of cardiac dysfunction that manifests clinically only after the myocardium is stressed. In short, we propose that SIC is another example of an occult cardiomyopathy with a distinct physiological trigger and suggest that alternative clinical approaches to these patients may be warranted. ABBREVIATIONS: CADD, Combined Annotation Dependent DepletionFPKM, fragments per kilobase pair of exon per million fragments mappedNHLBI GO ESP, National Heart, Lung, and Blood Institute Grand Opportunity Exome Sequencing ProjectPCR, polymerase chain reactionSIC, stress-induced cardiomyopathy.

Balloon-pump counterpulsation for management of severe cardiac dysfunction after aneurysmal subarachnoid hemorrhage.

OBJECTIVE: To evaluate the use of intraaortic balloon pump (IABP) placement to counter severe cardiac dysfunction after aneurysmal subarachnoid hemorrhage (SAH). METHODS: From August 2006 to October 2011, eight patients (seven women, mean age 47 years ± 5) with aneurysmal SAH underwent IABP placement. The modified Rankin scale (mRS) was used to assess outcome at discharge and long-term follow-up. RESULTS: Most patients presented in poor Hunt & Hess grade (grade III, 25%; grade IV, 62.5%; grade V, 12.5%). Three patients underwent surgical clipping, and five patients underwent endovascular treatment. All patients had severe cardiogenic shock, with a mean ejection fraction of 21%. One patient (12.5%) experienced transient left leg ischemia attributable to the IABP. No patient deaths occurred. At discharge, one patient was moderately disabled (mRS = 3), two patients were moderately to severely disabled (mRS, 4), and five patients were severely disabled (mRS = 5). The seven patients available for long-term follow-up (mean, 11.25 months) showed substantial functional improvements. Two patients exhibited no significant disability (mRS = 1), two patients exhibited only slight disability (mRS = 2), and 3 patients exhibited moderate to severe disability (mRS = 4). CONCLUSIONS: In select patients, particularly young women with poor-grade SAH, balloon-pump counterpulsation may serve as a useful adjunct in the management of severe cardiac dysfunction after SAH. Further investigation is necessary to define the optimal patient population for this technique.