Initial Diagnosis and Management of Coma

https://doi.org/10.1016/j.emc.2016.06.017Get rights and content

Section snippets

Key points

  • Coma is a life-threatening process that requires immediate stabilization and a structured approach to diagnosis and management.

  • The differential diagnosis for coma is long, but is often divided into structural vs. diffuse neuronal dysfunction; the latter is subdivided into toxic vs. metabolic.

  • When available, historical information may be of great use in determining the etiology of coma; in all cases, a focused physical examination can help greatly refine the differential diagnosis.

  • The definitive

Pathophysiology

A neuronal network in the dorsal pons and midbrain give rise to the ascending reticular activing system (ARAS), which is responsible for arousal.1 Neurons from these centers run together through the thalamus and then to the bilateral cerebral cortex; the cortex controls sensory processing and understanding, which generates awareness.2, 3 Coma results from an impairment of this axis by a process that affects the brain’s arousal center, consciousness center, the tracts that connect them, or some

Causes

A causal overview of coma is presented in Table 1, categorized based on this logic, and includes coma mimics, which are several disorders that may be easily mistaken for coma but do not involve interruption of the ARAS-thalamic-cortical pathway. For the purposes of this article, the focus is on relatively common entities that may present with coma, rather than those that are uncommon or in which coma is a late finding.

Tumors

Tumors may cause coma by exerting pressure on either a key area (eg, the brainstem) or by causing a diffuse increase in intracranial pressure. More commonly, however, patients with tumors have a slow progression of neurologic findings. Abrupt onset of coma in such patients often results from hemorrhage into an expanding mass. Even small tumors, however, may cause obstructive hydrocephalus or focal infarctions, each of which may in turn lead to the relatively abrupt onset of coma.

Acute Hydrocephalus

There is

Respiratory Insufficiency

Respiratory insufficiency may produce coma in two ways. First, the brain is particularly sensitive to the effects of hypoxia, with coma possible within minutes of acute oxygen deprivation. Second, hypercarbia may cause coma; the exact mechanism is unclear, but may involve an alteration in neurotransmitter levels or changes in intracranial pressure as increases in carbon dioxide levels are associated with increases in cerebral blood flow.

Dysthermia

Extremes of body temperature may accompany other primary

Sedative-Hypnotic Agents

Sedative-hypnotic agents are a broad class of drugs that include ethanol, benzodiazepines, barbiturates, baclofen, gamma-hydroxybutyrate, and others. Most sedative-hypnotic agents act by facilitating the effect of the neurotransmitter gamma-aminobutyric acid (GABA), hyperpolarizing neurons either through an increase in chloride conductance (GABAA)39 or through an increase in potassium conductance (GABAB).40 Ethanol, in addition to interacting with the GABA system,41 also produces some effects

Initial stabilization

The initial stabilization of comatose patients is the same as that for that of all emergency department patients and consists of securing the patients airway (with attention to the cervical spine), breathing, and circulation.

Decisions regarding airway management are often very difficult, driven by gestalt rather than algorithmic decision making, and are based on several factors. Mechanism of coma is important; although a GCS of 8 or less in a trauma patient is often viewed as an indication for

History

Comatose patients by definition cannot give details of their illness, so it is crucial that the provider actively seek alternative sources of information. Emergency medical service responders often provide the most valuable information. They can relay information obtained from family members or bystanders, describe the patient’s initial level of consciousness and how that has changed en route, provide a description of how the patient was found, and contribute important situational information

Physical examination

A complete physical examination will provide clues to the diagnosis of coma and help streamline the patient’s diagnostic evaluation. Crucial physical examination findings, and the important causes of coma associated with them, are listed below.

Pulse

Bradycardia may occur in the context of sympatholytic drugs, such as clonidine; in the setting of sedative hypnotic toxicity, particularly with barbiturates and gamma-hydroxybutyrate; and with increases in intracranial pressure, characteristically accompanied by systemic hypertension. Tachycardia is common with psychotropic drug poisoning, ketamine intoxication, adrenergic hyperactivity from intracranial hemorrhage, and 3,4-methylenedioxymethamphetamine (MDMA) intoxication, which produces coma

Imaging and laboratory testing

Although a thorough history and physical examination will often generate a refined differential diagnosis, imaging studies and laboratory testing play an important role in the diagnosis of coma. Such interventions, however, should serve to refine clinical impressions and should not be ordered indiscriminately as a substitute for thoughtful patient evaluation.

When coma is obviously caused by diffuse neuronal dysfunction, such as hypoglycemia or a known ingestion, CT is rarely if ever necessary.

Grading systems

Grading systems allow providers to quickly convey a general sense of the patient’s condition. This is particularly important when one provider cannot examine the patient, as may occurs in telephone discussions between providers or during emergency medical service communications.

Two major grading systems are used to assess the depths of coma (Table 3). The GCS, first described in 1974,76 is a 15-point composite score of eye, motor, and verbal responses developed to assess patients with head

Treatment

The ultimate treatment of coma depends on the cause. In general, there are three overarching themes regarding the treatment of coma.

First, coma from structural causes may be catastrophic and untreatable. However, when the cause is treatable, it can be treated surgically or with geographically targeted pharmacologic or mechanical intervention. The authors advocate for the early involvement of neurosurgical specialists for patients with coma from intracranial hemorrhage or hydrocephalus because

Summary

Coma represents a true medical emergency. Although drug intoxications are a leading cause of coma in patients who present to the emergency department, other metabolic disturbances and traumatic brain injury are common causes as well. The general emergency department approach to the patient with coma begins with stabilization of airway, breathing, and circulation, followed by a thorough physical examination to generate a limited differential diagnosis that is then refined by focused testing.

First page preview

First page preview
Click to open first page preview

References (82)

  • M. Miyasaka et al.

    Neural mechanisms of ketamine-induced anesthesia

    Int J Neuropharmacol

    (1968)
  • S.N. Caroff et al.

    Neuroleptic malignant syndrome

    Med Clin North Am

    (1993)
  • R. Duncan et al.

    Decreased Glasgow Coma Scale score does not mandate endotracheal intubation in the emergency department

    J Emerg Med

    (2009)
  • H.E. Williams

    Alcoholic hypoglycemia and ketoacidosis

    Med Clin North Am

    (1984)
  • M. Liu-Shindo et al.

    Basilar skull fractures in children

    Int J Pediatr Otorhinolaryngol

    (1989)
  • S. Forsberg et al.

    Metabolic vs structural coma in the ED–an observational study

    Am J Emerg Med

    (2012)
  • M.C. Brouwer et al.

    Dilemmas in the diagnosis of acute community-acquired bacterial meningitis

    Lancet

    (2012)
  • G. Teasdale et al.

    Assessment of coma and impaired consciousness. A practical scale

    Lancet

    (1974)
  • B.L. Edlow et al.

    Neuroanatomic connectivity of the human ascending arousal system critical to consciousness and its disorders

    J Neuropathol Exp Neurol

    (2012)
  • S. Sarasso et al.

    Quantifying cortical EEG responses to TMS in (un)consciousness

    Clin EEG Neurosci

    (2014)
  • E.F.M. Widjicks

    The comatose patient

    (2014)
  • P.B. Gorelick et al.

    Headache in acute cerebrovascular disease

    Neurology

    (1986)
  • D.J. Gaucher et al.

    Subdural hematoma following lumbar puncture

    Arch Intern Med

    (2002)
  • J.D. Miller et al.

    Acute subdural hematoma from bridging vein rupture: a potential mechanism for growth

    J Neurosurg

    (2014)
  • H. Maxeiner et al.

    Pure subdural hematomas: a postmortem analysis of their form and bleeding points

    Neurosurgery

    (2007)
  • P. De Bonis et al.

    Antiplatelet/anticoagulant agents and chronic subdural hematoma in the elderly

    PLoS One

    (2013)
  • M.R. Bullock et al.

    Surgical management of acute epidural hematomas

    Neurosurgery

    (2006)
  • R. Mayr et al.

    The impact of coagulopathy on the outcome of traumatic epidural hematoma

    Arch Orthop Trauma Surg

    (2012)
  • M.I. Aguilar et al.

    Spontaneous intracerebral hemorrhage

    Semin Neurol

    (2010)
  • D.J. Brown et al.

    Accidental hypothermia

    N Engl J Med

    (2012)
  • A. Bouchama et al.

    Heat stroke

    N Engl J Med

    (2002)
  • S. Strandgaard et al.

    Cerebral blood flow and its pathophysiology in hypertension

    Am J Hypertens

    (1989)
  • N.C. Schloot et al.

    Risk of severe hypoglycemia in sulfonylurea-treated patients from diabetes centers in Germany/Austria: how big is the problem? which patients are at risk?

    Diabetes Metab Res Rev

    (2016)
  • M. Kurien et al.

    A nationwide population-based study on the risk of coma, ketoacidosis and hypoglycemia in patients with celiac disease and type 1 diabetes

    Acta Diabetol

    (2015)
  • F.J. Pasquel et al.

    Hyperosmolar hyperglycemic state: a historic review of the clinical presentation, diagnosis, and treatment

    Diabetes Care

    (2014)
  • R.H. Sterns

    Disorders of plasma sodium–causes, consequences, and correction

    N Engl J Med

    (2015)
  • S.B. Legrand

    Modern management of malignant hypercalcemia

    Am J Hosp Palliat Care

    (2011)
  • S. Ben-Asuly et al.

    Coma due to hypercalcemia in a patient with Paget's disease and multiple parathyroid adenomata

    Am J Med Sci

    (1975)
  • M.J. Lucas et al.

    Outcome in patients with bacterial meningitis presenting with a minimal Glasgow Coma Scale score

    Neurol Neuroimmunol Neuroinflamm

    (2014)
  • T.D. Singh et al.

    The spectrum of acute encephalitis: causes, management, and predictors of outcome

    Neurology

    (2015)
  • N. Adam et al.

    Sepsis-induced brain dysfunction

    Expert Rev Anti Infect Ther

    (2013)
  • Cited by (12)

    • Median Nerve Stimulation Attenuates Traumatic Brain Injury–Induced Comatose State by Regulating the Orexin-A/RasGRF1 Signaling Pathway

      2022, World Neurosurgery
      Citation Excerpt :

      Up to 14% of patients with TBI enter into a long-duration coma state, whose duration is positively correlated with mortality after TBI.2,3 The pathogenesis of coma is currently assumed to be due to damage of the superior reticular activating system and alterations of the systems that maintain sleep arousal.4-6 Previous studies have suggested that median nerve stimulation (MNS) is an effective clinical treatment to induce coma emergence.

    • Diagnostic and prognostic EEG analysis of critically ill patients: A deep learning study

      2022, NeuroImage: Clinical
      Citation Excerpt :

      Acute consciousness impairment (ACI) represents a particular challenging condition for neurologists and intensive medicine specialists. Caregivers try to identify the underlying etiology in order to implement specific treatments (Edlow et al., 2014; Traub and Wijdicks, 2016); in case of delayed recoveries, there is need to estimate the chances that the patient will recover (Ramos et al., 2020; Sandroni et al., 2018). Both diagnostic and prognostic assessments are based on multimodal approaches (Edlow et al., 2014; Rossetti et al., 2016).

    • Independent risk factors for the development of incontinence-associated dermatitis (category 2) in critically ill patients with fecal incontinence: A cross-sectional observational study in 48 ICU units

      2018, International Journal of Nursing Studies
      Citation Excerpt :

      Table 1 describes the 23 potential risk factors studied. Cut-off values were established based on lab reference values, guidelines from the World Health Organisation (World Health Organization, 2011), scientific reports (Clyne and Olshaker, 1999; Patel and Kress, 2012; Traub and Wijdicks, 2016; van der Geest et al., 2016), and expert advice. The dependent variable was IAD category 2, defined as skin inflammation, due to contact with stool, manifested as skin erosion, denudation, or excoriation (Fig. 1) (Beeckman et al., 2017).

    View all citing articles on Scopus
    View full text