Hello, everyone. It is blink time. My name is Masan Desai. I'm an assistant professor in the Department of Neurology at the University of New Mexico. Today we're going to be discussing interesting cases in neurocritical care, highlighting brain-lung interactions. I have no disclosures relevant to this talk. Case one, we have a 62-year-old woman with a history of hypertension, epilepsy, chronic thrombocytopenia due to substance usage, who presented with headache, lethargy, left-gaze deviation, who subsequently became stuporous and was intubated for airway protection. Her initial GCS was a 10 with neurological deterioration, leading to a GCS of a 6. She was withdrawing to pain. Her vital signs initially demonstrated hypertension. She was tachycardic, initially hypoxic, and subsequently post-intubation, maintaining adequate saturations. CT had obtained on admission demonstrated diffused subarachnoid hemorrhage with global cerebral edema. Initial HNNS was 3 on admission, modified fissure of a 3 as well, with minimal intraventricular hemorrhage. Lab values demonstrated leukocytosis and thrombocytopenia. As a part of the next steps, antihypertensive drip to maintain systolic blood pressure goals less than 140 millimeters of mercury was initiated. Given thrombocytopenia, platelet transfusion was administered. And in the setting of an acute aneurysmal subarachnoid hemorrhage, antiseizure prophylaxis was enforced. Further imaging in the form of repeat CT had demonstrated re-bleeding, worsening hydrocephalus, global cerebral edema, and worsening in intraventricular hemorrhage. CT of the head demonstrated right pecomaneurysm as a source of patient's subarachnoid hemorrhage. On post-bleed day 1, digital subtraction angiogram was pursued, and the right pecomaneurysm was coiled successfully. Further during her clinical course, patient's exam improved, and she was successfully extubated on post-bleed day 3 with a GCSF of 14 post-extubation. On post-bleed day 5, patient's exam deteriorated, and she was lethargic, less responsive, and withdrawing to pain with a GCSF of an 11. Subsequently, she developed increase in the intracranial pressure up to 30 millimeters of mercury that were sustained with the very minimal CSF output. Repeat CT head was obtained to evaluate her deterioration clinically, which demonstrated worsening hydrocephalus, obstructed third ventricle, and worsening cerebral edema. She was bradycardic and hypertensive with declining saturations. To address her worsening hydrocephalus, she received a contralateral left ventricular external ventricular drain. Further in her clinical course, on post-bleed day 5 in the evening, she developed left arm and leg bledia when her systolic blood pressure drops from 140 millimeters of mercury to 90 millimeters of mercury. It was also noted that her hemoglobin dropped from a 9 to a 6 grams per deciliter. She was hypotensive, tachycardic. She had shallow breathing and hypoventilation. So the question was, what should be done next? As a part of the next steps, she was intubated for airway protection and also to avoid hypercarbia in the setting of a dynamic brain injury. Adequate access was obtained, including a central line for pressors. Given her hypovolemia and hemorrhagic shock concerns, blood products were initiated empirically. Given her clinical and neurological deterioration, CT of the head was pursued for her left-sided hemiplegia, which demonstrated diffused ways of spasm. With blood pressure augmentation, there was an improvement in her left-sided weakness. Melana was noted on the exam. Repeat laboratory findings demonstrated consumptive coagulopathy and decompensated liver failure. CT abdominal pelvis pursued to assess the underlying etiology of her hemorrhagic shock demonstrated esophageal varices. She received transfusions, however, continued to drop her hemoglobin and needing escalation of pressure requirements, which prompted a GI consultation, who recommended an upper GI endoscopy as a stat procedure. EGD demonstrated duolofoil lesions in the fundus of the stomach, which were clipped. There was evidence of minor varices as well. During the attempt to clip the duolofoil lesions, the patient lost up to four liters of blood in the form of an arterial hemorrhage. MTB protocol was initiated with worsening pressure requirements. After second round of MTB protocol transfusion, patient demonstrated worsening lung compliance with evident elevated peak and plateau pressures at bedside and abdominal distension concerning for an abdominal compartment syndrome. With ongoing massive transfusion protocol, there was worsening in patient's lung compliance with evidence of circulatory overload and lung injury associated with transfusion and presence of abdominal compartment syndrome, which led to a decline in patient's ventilation and perfusion status. Point-of-care ultrasound demonstrated B-lines. There was drop in patient's urine output due to the increase in the abdominal pressure. Transfusion was pursued from above and below, and diuresis was initiated. In the setting of hypoxia due to patient's worsening lung compliance, there was an evidence of difficulty in bagging the patient and frothy sputum on exam, which prompted further diuresis. Subsequently, the patient was evaluated by IR to make sure there was no active bleeding. In the setting of a dynamic cerebral disease state, vasospasm period, and disorder regulation, patient demonstrated evidence of worsening lung compliance with elevated peak and plateau pressures. Her ventilator settings demonstrated a tidal volume of 400 and respirator of 28 with a PACO2 of 42. Even though her ideal body weight was 40 kgs, she would not benefit from a drop in her tidal volumes due to concerns of hypercarbia. She required an FIO2 of 90% and a PEEP of 12 to deliver a PO2 of 57. There was concern of increasing the PEEP, which could lead to an increase in the intracranial pressure, again in the setting of a dynamic cerebral disease state. Special consideration that this case related to worsening secondary brain injury in the setting of concerns of increasing intracranial pressure and delivered cerebral ischemia in the vasospasm period. Systemic concerns of hypovolemia or VQ mismatch in the setting of a hemorrhagic shock and massive transfusion requirements can precipitate secondary brain injury. Low PEEP or optimal PEEP strategy, which balances patient's worsening lung compliance, increased abdominal pressure, and is based on brain tissue and perfusion markers should be instituted. Decompression of the abdomen can lead to improvement in the lung compliance. There is a concern of a drop in the patient's cerebral blood flow and cerebral perfusion pressure in the setting of an elevation of the intracranial pressure. Individualized PSCO2 and PO2 targets based on ICP and brain tissue monitoring should be instituted. There should be avoidance of intravascular depletion in the vasospasm period, which can precipitate delivered cerebral ischemia. When there is limited exam due to need for sedation and paralysis, dynamic cerebral monitoring tools, such as continuous EEG monitoring or NEERS, can be instituted as surrogates for secondary brain injury. In the setting of systemic hypovolemia, such as in this case with hemorrhagic shock, there can be perspiration of DCI or cerebral infarcts due to decline in cerebral perfusion pressure or cerebral blood flow. Neurological monitoring is an important strategy in this patient who has a limited exam. It can provide different data points for both cerebral and systemic perfusion and disease states, which can optimize cerebral and systemic hemodynamics and might influence outcomes in this patient and prevent secondary worsening and secondary brain injury. Teaching points from this case, we should optimize neurological exam to the best of our abilities. In the setting of an unlimited exam, multimodal tools should be instituted to guide therapeutics. Brain-focused therapy includes avoiding hyper or hypocarbia, controlled breathing, addressing cerebral and systemic autoregulation, and avoiding hypoxemia. Optimization of cerebral venous drainage by external venous drain should be pursued, and intracranial pressure monitoring should be instituted in the setting of secondary brain injury when addressing systemic issues. Optimization of cerebral perfusion pressure is a key to avoiding secondary brain injury. When correcting coagulopathy, we should watch for signs of volume overload. Deep titration should be based on ICP monitoring and brain tissue monitoring strategies. Conservative fluid management and resuscitation strategies should be instituted. Moving on to case two, we have a 24-year-old man who presented after a fall off a cliff with severe tibia and a seven-arch fracture. GCS on presentation is a four with pin-point pupils on exam and de-severed posturing. CT head demonstrates bifunctal and temporal blooming confusions. An intraparenchymal monitor is placed for ICP monitoring, demonstrating elevated ICPs, which are sustained, needing escalation of ICP management, including sedation, paralytics, and pentobarb due to refractory intracranial hypertension, which is persistent on hospital day four. It requires vasopressors to augment maps and optimize cerebral perfusion pressure in the setting of elevated intracranial pressure. Patient's clinical course is complicated by septic shock, worsening hypoxic respiratory failure because of an emesis in pneumonia, chest x-ray demonstrating worsening bilateral opacities. Low tidal volume minute ventilation is instituted, but leads to permissive hypercapnia, which subsequently causes increase in the intracranial pressure. Increasing tidal volume back to 7 cc per kg was not tolerated because increase in static pressures. Sedation and paralysis is initially sorted for control of increase intracranial pressure, but also helps achieve ventilator synchrony. Increase in the PEEP is instituted to 16 centimeter of water, which improves PO2 slightly, but results in refractory intracranial pressure elevations. On hospital day five, decision is made to prone the patient, and he remains prone for three days. Before performing this procedure, spine team is consulted to be present at bedside. A soft massage pillow is placed under his shoulders so that the cervical collar can remain. ICPs rise transiently during the first proning, but improve with institution of the hyperosmolar therapy. Reverse strangle position and addition of pillows under the chest and the hip is instituted to relieve abdominal pressure, which helps us elevate intracranial pressures. Prior to subsequent proning, hyperosmolar therapy and addition of sedation is instituted prophylactically for ICP control. No further ICP elevations are noted during the hospital course. Hypoxemia and hypercapnia improve substantially with proning, and by hospital day eight, no further ICP treatments are required for this patient. Teaching points for case two. Hypercapnia because of low tidal volume and ventilation can cause increase in intracranial pressure, which can subsequently escalate needs for other ARDS treatment. Increase in PEEP can result in ICP spikes. Cervical pressure optimization using vasopressors and conservative fluid management strategies should be instituted. Proning may be feasible in patients with spine injury. Consultation with the spine team to assess cervical spine stability and risk of proning should be pursued as a standard of care in these patients. Proning may be feasible in patients with increase in intracranial pressure, and ICP monitors should guide therapy. Proning can cause increase in the intracranial pressure. The following recommendations should be used to address this, which include optimization of ventilator settings, positioning maneuvers in addition to hyperosmolar therapy. I would like to thank and acknowledge all my colleagues who assisted me in preparing this presentation.

case studies

subarachnoid hemorrhage

neurocritical care

cerebral edema

elevated intracranial pressure