Signs of Concussion and Head Injury: Emergency Management

Introduction

Definition and Overview

Concussion is a form of mild traumatic brain injury (mTBI) characterized by transient neurological dysfunction following mechanical forces applied to the head or body. Head injury, in a broader sense, encompasses a spectrum ranging from superficial contusions to severe intracranial hemorrhage. Both conditions frequently present in emergency settings and demand rapid identification of clinical signs that predict progression or complications.

Historical Background

Early descriptions of concussive phenomena date to ancient physicians who noted “sudden loss of mind” following blows to the head. The formal adoption of the Glasgow Coma Scale (GCS) in the 1970s provided a standardized metric for assessing consciousness and has since guided triage protocols. Over recent decades, imaging modalities and pharmacologic adjuncts have refined emergency management, yet the core signs remain unchanged.

Importance in Pharmacology and Medicine

Recognition of subtle signs informs decisions regarding analgesia, sedatives, and anticonvulsants. Pharmacologic agents must be selected with caution to avoid exacerbation of intracranial pressure (ICP) or compromise of cerebral perfusion. Consequently, medical and pharmacy trainees must be conversant with both diagnostic criteria and therapeutic implications.

Learning Objectives

• Identify the key clinical manifestations associated with concussion and acute head injury.
• Understand the pathophysiological mechanisms that give rise to these signs.
• Evaluate pharmacologic considerations in the emergency treatment of head trauma.
• Apply evidence‑based decision trees to manage patients presenting with varying severities.
• Analyze case scenarios to integrate clinical assessment with therapeutic strategy.

Fundamental Principles

Core Concepts and Definitions

• Concussion: A functional disturbance of brain tissue without overt structural damage, typically reversible within hours to days.
• Intracranial Hemorrhage: Accumulation of blood within cranial compartments (parenchymal, subdural, epidural, subarachnoid).
• Glasgow Coma Scale (GCS): A three‑component score assessing eye opening, verbal response, and motor response; totals range from 3 to 15.
• Rehabilitation Potential: The likelihood that neurological deficits will resolve with appropriate care.

Theoretical Foundations

Mechanical forces impart rotational and translational acceleration to the brain. The resulting shear stress can disrupt axonal membranes, precipitating a cascade of ionic shifts, excitotoxicity, and metabolic failure. The brain’s autoregulatory capacity is challenged by increased ICP, which reduces cerebral perfusion pressure (CPP). CPP can be approximated by the equation: CPP = MAP − ICP, where MAP denotes mean arterial pressure. Maintaining CPP ≥ 60 mmHg is essential to prevent secondary ischemia.

Key Terminology

• Loss of Consciousness (LOC): Transient loss of awareness, often brief in concussion but may be prolonged in severe head injury.
• Arousal: The ability to respond to external stimuli; reduced arousal may indicate increased ICP.
• Neurological Deficit: Any focal loss of function (motor, sensory, visual) attributable to brain injury.
• Post‑Concussion Syndrome: Persistent symptoms such as headache, dizziness, and cognitive complaints beyond the acute phase.

Detailed Explanation

Mechanisms and Processes

Concussion involves a rapid acceleration‑deceleration event that generates shear forces across the cortical mantle. Axonal injury leads to neuronal depolarization and a surge in intracellular calcium. This biochemical milieu triggers the release of glutamate, a potent excitatory neurotransmitter, which, in excess, induces excitotoxic neuronal death. Simultaneously, cerebral blood flow may be transiently reduced, contributing to a hypoxic environment.

Mathematical Relationships and Models

Quantitative assessment of head injury severity can be modeled using the Injury Severity Score (ISS) and the Rotterdam CT score. The ISS aggregates anatomical injury scores across body regions: ISS = (AIS1)² + (AIS2)² + (AIS3)², where AIS denotes Abbreviated Injury Scale values. For head injury, the Rotterdam score assigns points based on midline shift, basal cistern status, and hemorrhage type, with higher scores correlating with poorer prognosis.

Factors Affecting the Process

• Age: Younger patients exhibit greater neuroplasticity but may also experience more severe diffuse axonal injury due to higher brain‑to‑skull volume ratio.
• Pre‑existing Conditions: Anticoagulants, antiplatelet agents, or hypertension can amplify bleeding risk and ICP elevation.
• Co‑trauma: Polytrauma increases systemic inflammatory responses, potentially exacerbating cerebral edema.

Clinical Significance

Relevance to Drug Therapy

Acute analgesia must balance pain control with ICP management. Non‑steroidal anti‑inflammatory drugs (NSAIDs) provide effective analgesia but carry a risk of platelet dysfunction, potentially worsening bleeding. Acetaminophen is often preferred in mild cases. Sedatives such as benzodiazepines are generally avoided due to the potential for respiratory depression and further ICP rise; however, in seizures secondary to focal hemorrhage, short‑acting agents like lorazepam may be justified.

Practical Applications

Standardized protocols, such as the Advanced Trauma Life Support (ATLS) airway–breathing–circulation (ABC) approach, incorporate early assessment of GCS, pupil reactivity, and neuroimaging. When imaging is unavailable, bedside neurologic examinations and the Canadian CT Head Rule guide decisions regarding computed tomography (CT) scans. In resource‑limited settings, the WHO guidelines recommend low‑dose CT or ultrasound when indicated.

Clinical Examples

• A 25‑year‑old athlete experiences a brief LOC following a football tackle. On examination, GCS is 15, pupils are equal and reactive, and no focal deficits are detected. A CT scan is deferred based on the Pediatric Head Injury Algorithm, and the patient is observed for 4 hours before discharge.
• A 68‑year‑old woman presents after a fall with nausea, vomiting, and a left occipital bruise. GCS is 13, left pupil is dilated, and she has a right‑sided hemiparesis. Immediate CT reveals a subdural hematoma with 5 mm midline shift. Surgical evacuation is pursued, and postoperative analgesia is managed with acetaminophen and cautious opioid titration.

Clinical Applications/Examples

Case Scenarios and Specific Drug Classes

1. Scenario A – Mild Concussion in a College Student
   • Assessment: GCS 15, no focal deficits, normal pupils, no vomiting.
   • Pharmacologic Consideration: Acetaminophen 1 g PO, repeated every 6 hours as needed for headache. NSAIDs are avoided due to potential platelet inhibition.
   • Follow‑Up: Education on return‑to‑activity guidelines and monitoring for post‑concussion syndrome.
2. Scenario B – Moderate Head Injury with Anticoagulation
   • Assessment: GCS 12, left pupil sluggishly reactive, CT shows a 3 mm epidural hematoma.
   • Pharmacologic Consideration: Vitamin K and fresh frozen plasma are administered to reverse warfarin therapy. Analgesia is limited to acetaminophen; opioids are avoided unless absolutely necessary.
   • Intervention: Neurosurgical consultation and possible craniotomy.
3. Scenario C – Severe Head Injury with Seizure Activity
   • Assessment: GCS 8, generalized tonic‑clonic seizure, CT shows intracerebral hemorrhage.
   • Pharmacologic Consideration: Lorazepam 4 mg IV, followed by levetiracetam 500 mg PO BID for seizure prophylaxis. Headache management includes acetaminophen; NSAIDs are contraindicated.
   • Monitoring: Continuous EEG, ICP monitoring, and serial imaging.

Problem‑Solving Approaches

• Apply the Canadian CT Head Rule to determine imaging necessity.
• Use the Glasgow Coma Scale to stratify patients into mild, moderate, and severe categories.
• Consider the patient’s medication profile, especially anticoagulants, before selecting analgesics.
• Integrate neuroimaging with clinical findings to decide on surgical intervention.

Summary / Key Points

• Concussion is a functional brain disturbance; head injury encompasses a spectrum of structural damage.
• Key clinical signs include loss of consciousness, altered consciousness, focal neurological deficits, and abnormal pupil reactivity.
• The Glasgow Coma Scale, CT imaging, and clinical prediction rules (e.g., Canadian CT Head Rule) guide management decisions.
• Pharmacologic therapy must account for ICP dynamics; acetaminophen is preferred for analgesia, NSAIDs are avoided, and sedatives are used cautiously.
• Early identification and appropriate intervention reduce morbidity and mortality; multidisciplinary collaboration is essential.

Clinical pearls for practitioners include maintaining a low threshold for imaging in patients with any focal deficit, avoiding antiplatelet or anticoagulant agents in the acute setting when possible, and monitoring for delayed signs such as increasing headache, vomiting, or new neurological deficits, which may herald secondary bleeding.

References

1. Walls RM, Hockberger RS, Gausche-Hill M. Rosen's Emergency Medicine: Concepts and Clinical Practice. 10th ed. Philadelphia: Elsevier; 2022.
2. Waller DG, Sampson AP. Medical Pharmacology and Therapeutics. 6th ed. Edinburgh: Elsevier; 2022.
3. Bennett PN, Brown MJ, Sharma P. Clinical Pharmacology. 12th ed. Edinburgh: Elsevier; 2019.
4. Feather A, Randall D, Waterhouse M. Kumar and Clark's Clinical Medicine. 10th ed. London: Elsevier; 2020.
5. Ralston SH, Penman ID, Strachan MWJ, Hobson RP. Davidson's Principles and Practice of Medicine. 24th ed. Edinburgh: Elsevier; 2022.
6. Loscalzo J, Fauci AS, Kasper DL, Hauser SL, Longo DL, Jameson JL. Harrison's Principles of Internal Medicine. 21st ed. New York: McGraw-Hill Education; 2022.
7. Rang HP, Ritter JM, Flower RJ, Henderson G. Rang & Dale's Pharmacology. 9th ed. Edinburgh: Elsevier; 2020.
8. Trevor AJ, Katzung BG, Kruidering-Hall M. Katzung & Trevor's Pharmacology: Examination & Board Review. 13th ed. New York: McGraw-Hill Education; 2022.