Weakness and/or Somnolence
Wendy E. Vaala • Guy D. Lester
Numerous conditions of the newborn foal can produce a primary complaint of weakness and/or somnolence. The gestational and postnatal age of the neonate should be established. If weakness has been present since birth, in utero–acquired bacterial or viral infections, birth asphyxia and trauma, chronic placental problems, and congenital anomalies should be placed higher on the list of differential diagnoses. Lethargy and loss of suckle are often the first signs of neonatal illness. A full udder on the dam accompanies poor nursing behavior in the neonate. If the neonate is somnolent and has injected mucous membranes and hyperemic coronary bands, sepsis is the primary differential and the most life threatening. If the neonate is relatively bright but is becoming progressively weaker, consider peripartum hypoxia and early signs of neonatal encephalopathy (NE). If the newborn shows signs of physical immaturity such as tendon laxity and silky hair coat, weakness may be due to fatigue, hypothermia, hypoxia, and/or hypoglycemia. Unfortunately, many weak foals begin to fade as a result of multiple problems. Glycogen branching enzyme deficiency in certain Quarter Horse and Paint lineages is an example of a genetic mutation associated with a range of abnormal signs that could include persistent recumbency.23
If weakness is present without accompanying somnolence, several other differentials should be considered, including trauma. If weakness is detected in one or more limbs immediately after birth, peripheral nerve and muscle damage associated with vigorous extraction from the birth canal should be ruled out. Affected limbs are weak and hyporeflexic, and there may be regions of cutaneous anesthesia.24 The diagnosis is based on history and neurologic assessment and confirmed using electrodiagnostics after 10 to 14 days.25 The prognosis for recovery is dependent on the severity of the neural lesion. Where axon continuity is preserved, the outlook is generally good with resolution within days to weeks; where there has been disruption to axons or whole nerves, the outlook is guarded. Regrowth and reinnervation of muscle is possible; axonal regrowth is estimated at 1 inch per month.25 Foals with rupture of the gastrocnemius muscle will be unable to rise or stand unsupported.26 The treatment includes limb stabilization and exercise restriction, with a guarded prognosis for an athletic career.
Neuromuscular diseases causing weakness without somnolence include botulism, nutritional myodegeneration (NMD; white muscle disease), and congenital myopathies. Botulism is an infection acquired via the gastrointestinal tract or through wounds or the umbilicus. Consequently, signs appear in neonates that are typically 10 days or older. Most cases of NMD associated with selenium and/or vitamin E deficiency occur during the first year of life among rapidly growing large animal neonates, but an in utero form of NMD may occur, resulting in clinical signs in affected foals soon after birth. Clinical signs associated with NMD may include localized (dysphagia) or generalized paresis. Rhabdomyolysis in foals may be precipitated by stress such as sepsis or excessive periparturient hypoxia. Affected foals are reluctant to move, paretic, and occasionally dysphagic.27 Pelvic limb muscles are often palpably firm. Elevated serum creatine kinase and electrolyte disturbances of hyponatremia and hyperkalemia may be observed.
It should be determined whether drugs or anesthetics were administered to the dam before or at the time of delivery, as many agents cross the placenta and exert depressive and other adverse effects on the fetus. Phenylbutazone administered to normal pregnant mares crosses the placenta and results in substantial concentrations of phenylbutazone, and its active metabolite oxyphenbutazone, in the foal. Although clinical signs of phenylbutazone toxicity were not noted in the foals postnatally,28 adverse effects are possible, particularly if other problems are present. Neonatal depression induced by drugs is particularly important following cesarean section deliveries. Maternally administered anesthetics and analgesics can suppress respiration and heart rate in the newborn. In horses, both xylazine and detomidine cause maternal and fetal bradycardia and reduced cardiac output.29,30 These effects will cause a reduction in placental perfusion and fetal oxygenation. If the newborn shows depression associated with maternal administration of these drugs, an α2-adrenergic antagonist, such as yohimbine, can be given. Adverse reactions to adrenergic antagonists in adult horses have been reported, some of which were fatal.31
Weakly basic drugs, when given to the mare, tend to concentrate in the fetus. Diazepam is an example of such a drug that crosses the placenta rapidly and accumulates in the fetal circulation, resulting in lethargy, hypotonia, and hypothermia in the neonate following delivery. Flumazenil has been used to reverse the sedative effects of benzodiazepines. Maternal systemic illness of various types may also result in a weak newborn.
Many neonatal disorders are associated with severe electrolyte and metabolic derangements that may clinically manifest as weakness, including hypoglycemia, acidosis, hyponatremia, hypernatremia, or hyperkalemia. Such abnormalities may occur before or at the time of birth, and laboratory assessment of the weak newborn is essential for accurate diagnosis. Young foals with hypocalcemia can present with stiff gait, muscular tremor, tachycardia, sweating, muscular tremor, and recumbency.32 Profound weakness associated with metabolic acidosis is commonly observed in foals with diarrhea. Correction of the acidosis by rehydration or intravenous administration of bicarbonate usually produces rapid improvement.
A number of congenital bacterial, fungal, and viral infections that cause abortions and stillbirths may also result in the birth of a live, weak neonate. Clinical manifestations of fetal infections depend on the age of the fetus and virulence and trophism of the infecting agent.
Generally, weakness resulting from uroperitoneum, renal, and liver failure; postnatally acquired infections; and neonatal isoerythrolysis (NI) is not expected to appear during the first 24 hours of age. Rather, foals with NI are usually presented between 24 and 72 hours of age, foals with uroperitoneum at 2 to 5 days or older, and neonates with postnatally acquired infections most commonly at 2 to 5 days of age or older.
Paraplegia and tetraplegia are commonly associated with spinal cord compression. Compression of the spinal cord in neonates most commonly results from vertebral body malformations, osteomyelitis, or fractures. Occipitoatlantoaxial malformations (OAAMs) involve the occipital condyles of the skull and the first two cervical vertebrae.33 Generally vertebral body malformations occur sporadically, with genetic, nutritional, and/or environmental factors being implicated.34 Osteomyelitis and vertebral body abscess may be a sequel to bacteremia following neonatal sepsis or pneumonia. Rhodococcus equi vertebral body osteomyelitis, with or without associated pulmonary infection, has been reported in foals. Leukocytosis and hyperfibrinogenemia are commonly observed in neonates with vertebral body abscesses. In most instances vertebral abscesses do not infiltrate the pachymeninges, so the cerebrospinal fluid (CSF) either is normal or has a mild elevation of protein and or a mild pleocytosis.
A complete neurologic examination is an important component of the work-up of the weak neonate. In particular, it should be noted if the weakness is accompanied by signs of somnolence and diffuse cerebral disease. Limb reflexes should be tested to establish whether components of the spinal reflex pathways are involved in the disease process (sensory nerve, lower motor neuron, neuromuscular junction, muscle). For example, foals with severe spinal cord hemorrhage may have relatively normal mentation, but spinal reflexes may be greatly diminished, and profound weakness may be present. Animals with other types of spinal cord disease (e.g., trauma, vertebral malformations) may also show weakness and ataxia yet have normal cerebral function.
Virtually any severe systemic disease such as generalized infection can cause both profound somnolence and weakness in a neonate without the presence of actual brain pathology. Primary neurologic disease in neonates is rare; commonly, neurologic dysfunction is associated with multisystemic disease. A thorough comprehensive physical examination and work-up is required to define a problem list and formulate an appropriate management plan. A complete blood count, blood cultures, and assessment of immunoglobulin status provide an indication of the likelihood of sepsis. Hypoxia and metabolic acidosis are ruled out by assessing arterial blood gas (ABG) status, and electrolyte disturbances and hypoglycemia are evaluated by measuring serum electrolytes and blood glucose concentration. Collection of CSF to assess the central nervous system is usually performed when disease in other organ systems that may account for the altered mental state has been ruled out and no improvement in the patient’s condition is observed following correction of electrolyte, blood gas, and metabolic derangements.