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Coma and Stupor 197

PEARLS & CONSIDERATIONS • Lattice-like hyperpigmentation is common distinctly brown rather than blue/purple on
with hypersensitivity dermatoses. a Diff-Quik preparation.
Comments
VetBooks.ir • When examining the nasal planum, look for • The best sites to biopsy the nasal planum (or SUGGESTED READING Diseases and Disorders
• Hyperpigmentation of the follicular ostia is
common with demodicosis.
changes in the surface architecture. Inflam-
Pigmentary abnormalities. In Miller WH, et al,
matory and infiltrative processes (e.g., discoid
lupus erythematosus) cause a loss of the other mucocutaneous junction) exhibiting editors: Muller & Kirk’s Small animal dermatology,
ed 7, St. Louis, 2013, Mosby, pp 618-629.
depigmentation are gray, partially depig-
normal cobblestone architecture. Conversely, mented areas. AUTHOR: Kinga Gortel, DVM, MS, DACVD
processes with little or no inflammation (e.g., EDITOR: Manon Paradis, DMV, MVSc, DACVD
vitiligo, snow nose) spare the normal surface Technician Tips
pattern. Abundant small, oval melanin granules can be
• Ventral depigmentation of the nasal planum seen in epithelial cells from surface cytologic
in dogs with nasal discharge may be associ- examination of hyperpigmented skin. Although
ated with aspergillosis. they can be mistaken for bacteria, they are

Coma and Stupor Client Education
Sheet

BASIC INFORMATION ability to elicit physiologic nystagmus, limb
rigidity, and respiratory patterns to determine Differential Diagnosis
Definition prognosis. • Intracranial: acute/rapidly progressive (e.g.,
A state of unconsciousness unresponsive to trauma, hemorrhage)
stimuli; an uncommon but well-recognized Etiology and Pathophysiology • Intracranial: chronic/slowly progressive (e.g.,
neurologic emergency • There are two general causes of tumor, abscess)
unconsciousness: • Infectious
Epidemiology ○ Diffuse cerebral cortical injury • Systemic disease
RISK FACTORS ○ Interruption of the ascending reticular • See Coma, Section 3 (p. 1206) for detailed
• Any condition that increases intracranial activating system located in the brainstem differential diagnosis.
pressure (ICP) • Diffuse cortical injury generally carries a
• Older animals: neoplasia, cardiovascular, better prognosis than brainstem injury. Initial Database
urinary disorders • Brainstem (midbrain, medulla) injury Laboratory tests:
• Younger animals: trauma, infection, toxins suspected based on • CBC (infection or thrombocytopenia)
• Traumatic brain injury most common cause ○ Deficits in pupillary light response or • Serum biochemistry panel (metabolic
in dogs and cats pupil size: midbrain (assuming exam disorders)
reveals no evidence of ocular or optic nerve • Urinalysis
CONTAGION AND ZOONOSIS lesion) ○ Glucose, ketones (diabetes mellitus/
Consider rabies ○ Inability to elicit normal physiologic ketoacidosis)
nystagmus: medulla (assuming no evidence ○ Calcium oxalate monohydrate crystals
Clinical Presentation of middle/inner ear abnormality on exam) (ethylene glycol intoxication)
DISEASE FORMS/SUBTYPES ○ Limb rigidity: medulla (assuming no spinal ○ Ammonium biurate crystals (portosystemic
• Prognosis is generally worse in descending cord or neuromuscular signs) shunt)
order ○ Respiration abnormalities: medulla or ○ Low urine specific gravity (USG)/casts
○ Obtunded: conscious state with mild to midbrain (barring primary airway/lung (renal disease [consider other causes of
moderate reduction in alertness lesion) low USG])
○ Stupor: unconscious state that requires ■ Kussmaul (rapid, deep, labored breath- • Prothrombin time/partial thrombo-
strong stimuli (usually noxious; toe pinch) ing, associated with diabetic coma) plastin time or activated clotting time
to evoke a response (often reduced) ■ Cheyne-Stokes (abnormal breathing (coagulopathies)
○ Coma: unconscious state unresponsive to pattern with alternating periods of • Serum bile acids (liver failure)
all stimuli apnea and deep, rapid breathing; the • Arterial blood gas analysis (hypoxemia,
cycle begins with slow, shallow breaths hypercarbia); alternative, SpO 2 and
HISTORY, CHIEF COMPLAINT that gradually increase in depth and rate capnography
• Acute onset or rapid deterioration: consider and are then followed by a period of Imaging, as suggested by history and
toxin, trauma, rapidly bleeding tumor, or apnea) examination:
embolism/infarction • Thoracic radiographs (metastatic lesions,
• Chronic slow progression: consider tumor, DIAGNOSIS trauma, or infections)
metabolic disease, or encephalitis • Skull radiographs (trauma/skull fractures)
Diagnostic Overview Arterial blood pressure (p. 1065)
PHYSICAL EXAM FINDINGS Suspected in any recumbent animal with no
• Recumbent with no response response on initial physical examination and Advanced or Confirmatory Testing
• May present in shock stimulation. Confirmed after a neurologic Magnetic resonance imaging (p. 1132) or
• Neurologic exam (p. 1136): focus on level examination that identifies the patient as computed tomography followed by cerebro-
of consciousness (response to toe pinch and recumbent and unresponsive to all stimuli spinal fluid analysis (pp. 1080 and 1323): after
loud noise), pupillary size and light reflexes, (including noxious stimuli). systemic disease is eliminated

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