Acute Traumatic Spinal Cord Injury & Neurogenic Shock

ABPN Neurocritical Care Study Guide Exam

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1 Chapter 1: Neurologic Examination & Coma Assessment in the ICU

Current Examination, Blueprint & Preparation Neurologic Examination in Critically Ill Patients Coma Evaluation & Consciousness Alterations Delirium & Toxic-Metabolic Encephalopathy in the ICU

2 Chapter 2: Cerebral Physiology & Intracranial Dynamics

Cerebral Blood Flow, Metabolism & Autoregulation Intracranial Pressure & Compliance Cerebral Edema & Herniation Syndromes

3 Chapter 3: Intracranial Hypertension & Cerebral Perfusion Management

Tiered ICP Management Protocols Hyperosmolar Therapy & Fluid Management Advanced & Refractory ICP Interventions

4 Chapter 4: Airway, Mechanical Ventilation & Pulmonary ICU Management

Emergency Airway Management & Neuro-Intubation Mechanical Ventilation Strategies in Acute Brain Injury Tracheostomy & Ventilator Weaning in Neurocritical Care Pulmonary Complications in the Neuro-ICU Obstructive Lung Disease, Pulmonary Hypertension & Bronchoscopy

5 Chapter 5: Hemodynamics, Shock & Cardiovascular Management

Hemodynamic Monitoring & Blood Pressure Targets Vasoactive Agents: Inotropes, Vasopressors & Antihypertensives Cardiac Complications of Brain Injury

6 Chapter 6: Neuropharmacology, Analgesia & Sedation

ICU Sedation & Analgesia Neuromuscular Blockade & Monitoring Propofol Infusion Syndrome & Drug Toxicities Antiseizure Drug Pharmacology in the ICU

7 Bleeding, Thrombosis & Hematologic Emergencies

Warfarin & Heparin Reversal Direct Oral Anticoagulant (DOAC) Reversal Antiplatelet Management & Platelet Dysfunction Venous Thromboembolism Prophylaxis & Management Transfusion, Coagulopathy, TMA & Cellular-Therapy Neurotoxicity

8 Chapter 8: Systemic ICU Care, Fluids, Electrolytes & Endocrine

Hyponatremia & Osmoregulation: SIADH vs Cerebral Salt Wasting Diabetes Insipidus, Hypernatremia & Endocrine Crises Critical Care Prophylaxis, Nutrition & Infection Prevention

9 Systemic Trauma & Environmental Injury

Polytrauma, Chest Injury & Abdominal Hemorrhage Burns, Electrical Injury & Hanging

10 Cardiac Emergencies & Mechanical Support

IABP, Ventricular Devices & ECMO Acute Coronary, Valvular, Rhythm & Aortic Emergencies

11 Kidney Injury, Acid–Base & Renal Replacement

Acute Kidney Injury & Renal Drug Clearance Acid–Base Disorders, Electrolytes & Renal Replacement

12 Systemic Infection & Endocrine Emergencies

Sepsis, Endocarditis & Antimicrobial Principles Thyroid, Adrenal & Dysglycemic Emergencies

13 Gastrointestinal & Hepatic Emergencies

Acute Abdomen, GI Bleeding & Abdominal Compartment Syndrome Acute Liver Failure, Cirrhosis & Hepatic Drug Effects

14 Chapter 9: Neuroimaging in the Neuro-ICU

Non-Contrast CT & CT Angiography CT Perfusion & Advanced Perfusion Imaging Magnetic Resonance Imaging in Critical Illness

15 Chapter 10: Electrophysiology & Neuromonitoring

Continuous EEG & ACNS Standardized Critical Care Terminology Invasive Neuromonitoring: ICP & External Ventricular Drains Multimodal Monitoring: PbtO2, Microdialysis & Transcranial Doppler

16 Angiography, Electrodiagnosis & CSF Analysis

Conventional Angiography & Cranial–Spinal Shunts EMG, Nerve Conduction & Acute Muscle Disease CSF Analysis: Infection, Inflammation & Hemorrhage

17 Chapter 11: Bedside Procedures, Ultrasound & Death by Neurologic Criteria

Critical Care Procedural Skills Critical Care Ultrasound & Echocardiography Determination of Death by Neurologic Criteria

18 Chapter 12: Acute Ischemic Stroke & Reperfusion Therapies

Acute Ischemic Stroke Management & Thrombolysis Endovascular Thrombectomy & Large Vessel Occlusion Malignant Hemispheric & Cerebellar Infarction

19 Chapter 13: Spontaneous Intracerebral Hemorrhage & Intraventricular Hemorrhage

Acute Intraparenchymal Hemorrhage Management Intraventricular Hemorrhage & Hydrocephalus Surgical Evacuation & Minimally Invasive Surgery in ICH

20 Chapter 14: Aneurysmal Subarachnoid Hemorrhage & Delayed Cerebral Ischemia

Aneurysmal Subarachnoid Hemorrhage: Acute Resuscitation & Securing Delayed Cerebral Ischemia & Cerebral Vasospasm Non-Aneurysmal Subarachnoid Hemorrhage & Vascular Malformations

21 Venous, Spinal & Traumatic Vascular Disease

Cerebral Venous Thrombosis & Spinal Cord Infarction Traumatic Dissection, Carotid–Cavernous Fistula & Penetrating Injury

22 Chapter 15: Traumatic Brain & Spinal Cord Injury

Severe Traumatic Brain Injury & Contusions Acute Traumatic Spinal Cord Injury & Neurogenic Shock Spine Trauma, Fractures & Cord Syndromes

23 Chapter 16: Status Epilepticus, Seizures & Neuromuscular Emergencies

Status Epilepticus: Convulsive & Non-Convulsive Refractory & Super-Refractory Status Epilepticus Acute Neuromuscular Respiratory Failure

24 Chapter 17: Post-Cardiac Arrest Care, CNS Infections & Encephalitis

Targeted Temperature Management & Post-Cardiac Arrest Care Post-Cardiac Arrest Neuroprognostication Acute CNS Infections, Encephalitis & Inflammatory Emergencies

25 Neuroinflammation & Neurooncology

Fulminant Demyelination & Autoimmune Encephalitis Brain, Spinal & Leptomeningeal Cancer Emergencies

26 Pregnancy, Transplantation & Pediatric Care

Pregnancy, Postpartum & Post-Transplant Neurologic Care Pediatric Neurocritical Care

27 Chapter 18: Neurosurgical & Perioperative Emergencies

Postoperative Neurosurgical Complications Device Complications: EVDs, Shunts & ICP Monitors Cerebral Hyperperfusion Syndrome & Post-Interventional Emergencies

28 Chapter 19: Ethics, Palliative Care & Organ Donation in the Neuro-ICU

Communication, Surrogate Decision-Making & Conflict Resolution Neuroprognostication Ethics, Withdrawal of Life Support & Palliative Care Organ Donation & Management of the Deceased Donor

Acute Traumatic Spinal Cord Injury & Neurogenic Shock

Key Takeaways Explain This Topic AI

Exclude hemorrhage and other causes before attributing trauma-associated hypotension to neurogenic shock.

The 2024 guideline weakly suggests MAP augmentation with a lower limit of 75–80 and upper limit of 90–95 mm Hg for 3–7 days; evidence is very low quality.

Early decompression within 24 hours is supported when feasible; no universal 8-hour requirement or steroid prerequisite applies.

Autonomic dysreflexia usually follows SCI at or above T6; identify bladder, bowel, skin, and other triggers while treating dangerous hypertension.

Last updated: October 2026

• Acute Spinal Cord Injury and Autonomic Disorders
• Initial Priorities

Prevent secondary spinal cord ischemia by maintaining oxygenation, ventilation, alignment, and systemic perfusion. Stabilize the airway with an approach that minimizes unnecessary cervical movement without sacrificing oxygenation. High cervical injuries can weaken the diaphragm, while lower cervical and thoracic injuries impair cough and secretion clearance. Serial respiratory mechanics, work of breathing, gas exchange, fatigue, and bulbar protection guide escalation; do not wait for profound hypercapnia before recognizing impending failure.

Treat hemorrhage and associated chest, abdominal, pelvic, or long-bone trauma in parallel. A warm extremity examination or bradycardia does not exclude bleeding. Obtain appropriate CT and selected MRI, assess compression and ligament injury, and involve spine specialists promptly. The neurologic examination should document motor, sensory, and sacral findings and be repeated after stabilization. Early decompression within 24 hours is supported when feasible, with timing individualized to physiologic stabilization and the operative lesion. A fixed 8–12-hour requirement is not a universal guideline mandate.

Neurogenic Shock Versus Spinal Shock

Neurogenic shock is circulatory failure from loss of sympathetic tone, often with higher cord injuries. Vasodilation, venous pooling, and impaired cardiac sympathetic output can produce hypotension with an inappropriately slow heart rate. Diagnose it after evaluating hemorrhage, obstructive shock, cardiogenic causes, drug effects, and other contributors. Give appropriate fluid for actual volume depletion and use vasoactive support when needed; excessive crystalloid can worsen pulmonary complications.

Norepinephrine is commonly used because it supports vascular tone and cardiac output. The 2024 SCI hemodynamic guideline did not establish one preferred vasopressor from adequate comparative evidence. Phenylephrine can worsen reflex bradycardia or reduce output in some patients, but it is not an absolute contraindication in every SCI. Treat clinically important bradyarrhythmia according to severity, with medication and pacing when indicated. Monitor rhythm, myocardial injury, extremity perfusion, and the effects of pressor escalation.

Spinal shock describes transient depression of reflex and motor activity below an acute cord lesion. It is not synonymous with hypotension. Early areflexia does not prove permanent lower motor neuron destruction or complete transection. Reflexes return in stages. The bulbocavernosus reflex is useful to document but its return does not establish that every component of spinal shock has resolved or that final prognosis is known.

Perfusion Augmentation and Evidence

The 2024 guideline weakly suggests augmenting MAP to at least a lower boundary of 75–80 mm Hg while avoiding active augmentation above an upper boundary of 90–95 mm Hg, for 3–7 days. These are ranges for selecting a clinical target, not an instruction to alternate between all numbers. The evidence is very low quality. An upper augmentation boundary does not mean lowering a patient's spontaneously higher MAP without another indication. Document the chosen goal, duration, response, and complications.

Prevent hypotension during transport, sedation, intubation, and surgery. Confirm arterial-line accuracy and reference level. An unexplained fall in pressure requires reassessment rather than automatically increasing a pressor. Excessive augmentation can cause arrhythmias, ischemia, or volume-related complications. Spinal cord perfusion concepts are important, but invasive intraspinal monitoring is not an established routine requirement for every patient.

High-dose methylprednisolone is not routine standard care for traumatic SCI. Recommendations have differed: the 2017 AO Spine guidance allowed a 24-hour infusion as an option in selected adults treated within eight hours, whereas other professional guidance recommends against use. It is not a prerequisite for decompression, is not recommended as a routine 48-hour course, and requires consideration of infection, bleeding, glucose, and other harms. Do not label every steroid exposure for another indication contraindicated because the patient has SCI.

Autonomic Dysreflexia

After SCI, particularly at or above T6, a noxious stimulus below the lesion may provoke abrupt severe hypertension with headache, flushing or sweating above the lesion, and sometimes reflex bradycardia. A substantial rise above a patient's low baseline can be clinically significant even before a conventional hypertension threshold is reached. Bladder distension or catheter obstruction is common; bowel impaction, pressure injury, tight clothing, fractures, and procedures are other triggers.

Sit the patient upright when safe, loosen restrictive items, monitor pressure frequently, and identify the trigger urgently. Inspect the urinary system for kinks or obstruction and manage according to the appropriate catheter protocol. Avoid escalating a painful bowel examination before controlling dangerous pressure and providing suitable measures. Short-acting antihypertensive treatment may be necessary under the local protocol. Check contraindications and recent phosphodiesterase inhibitor exposure before nitrate use. Persistent symptoms require a wider search, including other causes of hypertensive emergency. Continue observation because pressure can recur or fall after treatment.

Paroxysmal Sympathetic Hyperactivity

Severe acquired brain injury can cause recurrent simultaneous episodes of tachycardia, hypertension, tachypnea, hyperthermia, sweating, and motor posturing, often triggered by care. This is distinct from SCI-related autonomic dysreflexia. Exclude seizure, infection, pain, hypoxia, withdrawal, pulmonary embolism, and medication toxicity before labeling an episode a sympathetic storm. Serial pattern recognition and a structured assessment tool can help.

Reduce triggers, provide analgesia, manage temperature and hydration, and consider a coordinated combination of abortive and preventive medication. Opioids, alpha-2 agonists, beta blockade, gabapentin, and antispasticity agents have different roles and adverse effects; evidence does not identify one universal regimen. Avoid masking a new neurologic deterioration as a familiar storm without reassessment. Longer-term care also addresses thromboprophylaxis, pressure injury, bowel and bladder function, nutrition, respiratory hygiene, and rehabilitation.

Source: 2024 SCI hemodynamic guideline and ACS best-practice resources .

Decision Review

• Syndrome Main distinction
• Neurogenic shock Circulatory failure from loss of sympathetic tone
• Spinal shock Transient depression of reflex and motor activity below injury
• Autonomic dysreflexia Trigger-related hypertension after higher SCI
• Paroxysmal sympathetic hyperactivity Recurrent combined autonomic and motor episodes after brain injury