Hypertension In Intensive Care Unit Research Articles

Pulmonary hypertension in the intensive care unit after pediatric allogeneic hematopoietic stem cell transplant: incidence, risk factors, and outcomes.

To determine the incidence, risk factors, and outcomes of pulmonary hypertension (PH) in the pediatric intensive care unit (PICU) after pediatric hematopoietic stem cell transplant (HCT). This was a retrospective study of pediatric patients who underwent allogeneic HCT between January 2008-December 2014 at a center contributing to the Center for International Blood and Marrow Transplant Research data registry. Incidence of PH was assessed from PICU diagnostic codes from records merged from the Virtual Pediatric Systems database. Regression and survival analyses identified factors associated with post-HCT PH. Additional post-HCT morbidities and survival after PH were also assessed. Among 6,995 HCT recipients, there were 29 cases of PH, a cumulative incidence of 0.42% (95% CI 0.27%-0.57%) at 60 months post-HCT. In the sub-cohort of 1,067 patients requiring intensive care after HCT, this accounted for a PH prevalence of 2.72% (95% CI 1.74-3.69%). There was an increased risk of developing PH associated with Black/African American race, metabolic disorders, partially HLA-matched or cord blood allografts, graft-versus-host prophylaxis regimen, and lower pre-HCT functional status. Patients who developed PH had significant PICU comorbidities including heart failure, pulmonary hemorrhage, respiratory failure, renal failure, and infections. Survival at 6 months after diagnosis of post-HCT PH was 51.7% (95% CI 32.5%-67.9%). PH is a rare but serious complication in the pediatric post-HCT population. A significant burden of additional comorbidities, procedural interventions, and risk of mortality is associated with its development. Close monitoring and prompt intervention for this severe complication are necessary in this vulnerable population.

Management of Intracranial hypertension in Intensive Care Unit: A Literature Review

Intracranial hypertension (IH) is a common clinical problem in the intensive care unit (ICU) and critical care unit. IH is the result of increased intracranial pressure. High ICP can cause secondary brain injury and even death. The most common causes of increased ICP are trauma to the brain or skull and stroke. Commonly used barbiturates are pentobarbital and phenobarbital. Another method for decreasing ICP is to paralyze the patient using something like vecuronium. All the patients who are paralyzed MUST be sedated. We can also use paralytics for a patient for aggressive cooling in order to prevent shivering. Sometimes vasopressors are added in order to keep MAP high enough to maintain an adequate CPP.

Early rehabilitation by electrical muscle stimulation in intensive care unit for patients with intracranial hypertension

Japanese guidelines for the management of stroke recommend early rehabilitation for the prevention of disuse syndrome. However, there are few reports concerning the safety and risk of the rehabilitation for the patients with intracranial hypertension. The patients with intracranial hypertension cannot attempt to move their extremities, and ROM exercise without contraction of muscle tends to the main early rehabilitation in intensive care unit. It leads to disuse muscle atrophy. Therefore, we introduced belt electrode-skeletal muscle electrical stimulation (B-SES) as electrical muscle stimulation, which causes a muscle contraction, for patients with intracranial hypertension, and we assessed the safety of B-SES for the patients with intracranial hypertension. We use AUTO Tens PRO Rehabili Unit made by HOMER ION LABORATORY CO., LTD, and selected LEG DISUSE MODE, and the duration of the stimulation is 20 minutes. Physical therapist determined the output level by palpation of triceps surae muscle of each patient, and the effective intensity was usually between 20 V and 50 V. Case 1: a 43-year-old woman underwent coil embolization of the ruptured right VA-PICA aneurysm. We monitored her intracranial pressure (ICP) by external drainage, and her ICP kept 14.5–18.0 cmH 2 O during B-SES. Case 2: a 66-year-old man underwent external drainage for the acute hydrocephalus due to left thalamic hemorrhage and intraventricular hemorrhage. His ICP kept under 17.5–19.0 cmH 2 O during B-SES. Case 3: a 49-year-old man with right acute subdural hematoma underwent hematoma removal with decompressive craniotomy. His ICP kept 8–11 mmHg during B-SES. Case 4: a 41-year-old woman presented with subarachnoid hemorrhage underwent neckclipping of the left middle cerebral artery aneurysm. Her ICP kept 8–11 mmHg during B-SES. Electrical muscle stimulation with B-SES, as can be seen from these four cases, never worsened intracranial hypertension. Therefore, early rehabilitation with B-SES is safety and worth introducing for the patient with intracranial hypertension in intensive care unit.