Module - 5 - Neurological Emergencies Flashcards
- You are preparing to transport a twenty-year-old man weighing 200 pounds with a history of a self-inflicted gunshot wound to the head. He is intubated with A/C ventilator settings of FIO2 0.5, Vt 600, I/E 1:2, flow 5 L, RR 10, PIP 30. Vital signs are BP 100/60, HR 66, and SaO2 94%. ICP reading of 28. His cerebral perfusion pressure is approximately
A. 100 mmHg
B. 70-90 mmHg
C. 60 mmHg
D.
- D: The intracranial contents have three components: cerebrospinal fluid (CSF), blood volume, and the brain. As mean systemic arterial pressure increases, cerebral arterial blood vessels constrict, preventing the increase in blood volume and flow that would normally occur. If the mean systemic arterial blood pressure decreases, the cerebral arteries dilate, increasing cerebral blood flow. A mean systolic arterial pressure of approximately 60-140 mmHg, cerebral blood flow may be maintained in a constant state.
- What is the initial clinical presentation that may indicate that ICP may be increasing?
A. Hypotension
B. Deteriorating level of consciousness
C. Tachypnea
D. Tachycardia
- B: All neurologic emergencies can lead to coma. During patient assessment, it is useful to use a systematic approach in evaluating the comatose patient and establishing a baseline differential diagnosis. The Glasgow Coma Scale (GCS) is widely used to measure the severity of coma in patients and is therefore and indicator of prognosis.
- You are transporting an eighteen-year-old female patient with a history of being ejected from a motor vehicle accident. She is currently awake and oriented to person, place, and time; however, she is slow to respond. Vital signs are a BP of 70/42, HR 68, RR 26, SaO2 95%, temp. 98.8°F. Hemodynamic readings are CVP 3, CI 2.0, and SVR 600. ICP reading at 6 with a urine output of 100 mL over the last two hours. Your patient is exhibiting signs and symptoms of
A. Herniation
B. Hypovolemic shock
C. Spinal cord injury
D. Diabetes insipidus
- C: The patient is presenting with signs and symptoms of neurogenic shock: tachypnea, normal heart rate, and hypotension. Hemodynamic parameters to indicate the presence of neurogenic shock would include a decreased SVR
- You are transporting a forty-year-old male diagnosed with a subarachnoid hemorrhage. Which of the following assessment findings can be associated with his diagnosis?
A. Presence of doll’s eyes reflex
B. Positive Battle’s sign
C. Positive Brudzinski’s sign
D. Absence of ipsilateral pupillary dilation
- C: Positive Brudzinski’s sign can indicate the presence of a subarachnoid hemorrhage as well as meningitis. Severe neck stiffness causes the patient’s hips and knees to flex when the neck is flexed.
- You arrive on the scene to manage a fall victim. She presents with a BP 70/palp, HR 62, RR 24, Sats 96%. EMS reports brief LOC but now has a GCS of 14. You note a deformity of the right femur, and she is complaining of neck pain. The clinical presentation is most likely a diagnosis of
A. Neurogenic shock
B. Hypovolemic shock
C. Epidural bleed
D. Subdural bleed
- A: Spinal cord injury can lead to neurogenic shock. The patient is presenting with tachypnea, hypotension, and a normal heart rate but can also be present with bradydysrhythmias because of loss of sympathetic tone secondary to the spinal cord injury.
- Pupillary dilation in response to the oculomotor nerve insult that occurs in uncal herniation is a result of
A. Loss of parasympathetic stimulation
B. Loss of sympathetic stimulation
C. Parasympathetic overstimulation
D. Sympathetic overstimulation
- A: The innermost part of the temporal lobe, the uncus, can be compressed so that it goes by the tentorium and places pressure on the brain. The uncus can compress the third cranial nerve, which can affect the parasympathetic input to the eye on the side of the affected nerve, causing the pupil on the affected side to dilate and fail to constrict in response to light as it should.
- Which formula can be used when calculating a cerebral perfusion pressure (CPP)?
A. [(DBP × 2) + SBP] divided by 3
B. MAP − ICP
C. ICP − DBP
D. [(DBP + 2) × SBP] divided by 3
- B: MAP − ICP = CPP.
- An early sign of tentorial herniation would be
A. Doll’s eyes reflex
B. Ataxic breathing
C. Paralysis below the diaphragm
D. Ipsilateral pupillary dilation
- D: Ipsilateral pupil dilation on the affected side.
- You have been requested to transport a thirty-two-year-old male involved in a two-car motor vehicle collision in which the right side of his head struck the “A-post.” Right middle meningeal artery damage has been noted by CT with right-sided “mass effect” resulting. You would expect which of the following?
A. Epidural hematoma
B. Ventricular collapse
C. Cranial midline shift to the left
D. All of the above
- D: All of the above. The middle meningeal artery runs in a groove on the inside of the cranium beneath the pterion, which is vulnerable to injury at this point, where the skull is thin. A blow or fracture of the temporal bone is often the cause of a rupture of the middle meningeal artery, which may cause an epidural hematoma (occurs between the skull and the dura). There is often significant “mass effect” with compression of the ipslateral lateral ventricle and dilatation of the opposite lateral ventricle due to obstruction of the foramen of Monro. Emergency treatment requires decompression of the hematoma, usually by craniotomy.
- The patient presents with a skull fracture that appears to have a central focal point with multiple fractures outward on radiography. This skull fracture would be described as
A. Linear
B. Linear stellate
C. Diastatic
D. Depressed
- B: Linear stellate is a skull fracture with multiple linear fractures radiating from the site of impact. A growing skull fracture (GSF) also known as a craniocerebral erosion or leptomeningeal cyst due to the usual development of a cystic mass filled with cerebral spinal fluid is a rare complication of head injury usually associated with linear skull fractures of the parietal bone in children below three years of age. There are four major types of skull fractures: linear, compressed, distatic, and basilar.
- A head-injured patient would most likely experience an increased ICP as a result of which action?
A. Hip flexion
B. Gagging on the ETT
C. Adduction of the arms
D. Rotation of the head
E. All of the above
- E: All of the above are considered movements/stimulators that can increase ICP. The intubated patient who is restless or who resists ventilatory support is increasing their ICP, which can be extremely critical. Seizures that develop during transport should be promptly treated because they produce hypoxia and cause increased ICP. Intravenous administration of benzodiazepines is indicated for initial seizure management. Hypotension has been found to contribute to the mortality and morbidity of head-injured patients. The patient’s mean arterial pressure (MAP) should be maintained at more than 90 mmHg. Fluids and blood products should be administered to maintain blood pressure.
- You are transporting an awake multisystem trauma patient from a small rural facility with the following vital signs: BP 200/66, HR 56, RR 20-36, SaO2 97%, and temp. 99.9°F. Further assessment reveals a large laceration to the occipital area of the head, with bleeding controlled, and is moving all extremities. Pupils are reactive to light and equal at 4 mm with extraocular movements intact. The patient’s clinical presentation is suggestive of which of the following?
A. Demonstrating signs/symptoms of cushing’s triad
B. Already herniated and will likely deteriorate further
C. Demonstrating signs/symptoms of Brown-Séquard syndrome
D. Demonstrating signs/symptoms of hypovolemic shock
- A: The clinical presentation of Cushing’s triad is the triad of widening pulse pressure (rising systolic, declining diastolic), change in respiratory pattern (irregular respirations), and bradycardia. It is a sign of increased ICP, and it occurs as a result of the Cushing reflex. The normal average range for ICP is 0-10 mmHg.
- You are transporting a thirty-year-old female who was involved in a single vehicle rollover two hours prior to your arrival. She has a swan catheter in place with the following values: CVP 2, CI 2.0, PA S/D 12/6, wedge 7, SVR 400. Vital signs: BP 80/48, HR 46, RR 24, SaO2 90%. The patient’s clinical presentation is suggestive of which diagnosis?
A. Hypovolemic shock
B. Septic shock
C. Left ventricular failure
D. Neurogenic shock
- D: The patient is presenting with neurogenic shock. The SVR
- The expected average normal cerebral perfusion pressure range (CPP) is
A. 80-100 mmHg
B. 50-60 mmHg
C. 70-90 mmHg
D. >100 mmHg
- C: Normal cerebral perfusion pressure range is 70-90 mmHg.
- The average normal ICP range is
A. 0-10 mmHg
B. 10-20 mmHg
C. 20-30 mmHg
D. >30 mmHg
- A: Normal ICP range is 0-10 mmHg, but range can go as high as 15 mmHg.
- The formula to calculate a mean arterial pressure (MAP) is
A. 2/3 DBP × SBP
B. [(DBP × 2) + SBP] divided by 3
C. [(SBP × 2) + DBP] minus 3
D. [(DBP + 2) × SBP] divided by 3
- B: MAP = [(DBP × 2) + SBP] divided by 3.
- The patient presents with the following hemodynamic parameters: CVP 1, CI 1.7, PA S/D 12/6, wedge 6, and SVR 300. Vital signs are 78/40, HR 60, RR 16, SaO2 98%. The most likely cause is
A. RVMI
B. Neurogenic shock
C. Septic shock
D. Hypovolemic shock
- B: SVR
- Classic picture of neurogenic shock presents with
A. Hypertension
B. Absence of tachycardia
C. Cool skin
D. Pallor
- B: Loss of sympathetic tone below the level of the injury results in loss of autoregulation, a decrease in vascular tone, and inability of the heart to increase its intrinisic rate. The classic picture of neurogenic shock presents with the absence of tachycardia.
- You are transporting a patient with a spinal cord injury above T6 level. His baseline vital signs prior to lift off: BP 160/80, HR 62, RR 20. During transport, the patient begins to complain of a throbbing headache with nasal stuffiness. Your assessment reveals that the patient is becoming increasingly agitated. His skin color is flushed and profusely diaphoretic. Repeat vital signs are a BP 206/100, HR 52, RR 26. Your initial management of the patient would be
A. Insert a foley catheter
B. Administer nitroglycerin to help reduce blood pressure
C. Hang a Nipride drip if diastolic is greater than 130 mmHg
D. Do nothing because increased HTN is expected with altitude and spinal cord injuries
- A: Autonomic dysreflexia (AD), also known as “autonomic hyperreflexia or hyperreflexia,” is a potentially life-threatening condition, which can be considered a medical emergency requiring immediate attention. AD occurs most often in spinal cord-injured individuals with spinal lesions above the T6 spinal cord level. Acute AD is a reaction of the autonomic (involuntary) nervous system to overstimulation. This condition is distinct and usually episodic, with the patient experiencing remarkably high blood pressure (often with systolic readings over 200 mmHg), intense headaches, profuse sweating, facial erythema (redness), flushing of the skin above the level of the lesion, goosebumps, nasal stuffiness, bradycardia, apprehension, anxiety, and a “feeling of doom.” An elevation of 40 mmHg over baseline systolic should be suspicious for dysreflexia. Catheterization of the bladder or relief of a blocked urinary catheter tube may resolve the problem. If the noxious precipitating trigger cannot be identified, drug treatment is needed to decrease elevated ICP until further studies can identify the cause.
- You have been requested to transport a forty-year-old male fall victim of approximately 25-30 feet, three hours prior to your arrival. Your assessment reveals a greater motor weakness in upper extremities than in lower extremities, with varying degrees of sensory loss. The clinical presentation may suggest which of the following spinal cord syndrome?
A. Brown-Séquard
B. Central cord
C. Anterior cord syndrome
D. Neurogenic shock
- B: Central cord syndrome is the most common spinal cord injury (SCI) syndrome. This syndrome is unlike a complete lesion and causes loss of all sensation and movement below the level of the injury. Remember “you can dance, but you can’t clap.”
- Hypothermia, low levels of 2,3-DPG, and hypocarbia can cause the oxyhemoglobin dissociation curve shift to go
A. Up
B. Down
C. Right
D. Left
- D: A left shift causes an increase in the affinity, making the oxygen easier for the hemoglobin to pick up but harder to release. Refer to the table for review of causes.
- In addition to glucose, which electrolyte must be maintained within normal limits when managing a head-injured patient?
A. Calcium
B. Magnesium
C. Potassium
D. Sodium
- D: Low serum sodium levels following traumatic brain injury (TBI) can lead to extracellular volume depletion and cerebral edema. These can all result in dangerous increases in ICP. Hypertonic saline can help avoid the negative effects of hyponatremia by increasing serum sodium levels in the acute phase of head trauma care (Johnson and Criddle, 2004; Suarez, 2004). Maintaining serum sodium levels of 145-155 mmol/L is likely to achieve this goal. Serum sodium levels should be maintained no higher than 155 mmol/L. Higher levels are dangerous. Patients with serum sodium levels higher than 160 mmol/L are at increased risk for treatment-related renal failure, pulmonary edema, and heart failure. If serum sodium levels remain above 160 mmol/L for more than 48 hours, the risk of these problems increases even more. Furthermore, if serum sodium levels climb beyond 160 mmol/L, patients are at risk for seizures. The target serum osmolarity is less than 320 mOsmol/L. At higher levels, patients are at increased risk for treatment-related renal failure (Qureshi and Suarez, 2000; Suarez, 2004).
- You are transporting a twenty-year-old male, with penetrating head and facial trauma. During transport, the patient complains of a severe headache, nausea, and vertigo. Your assessment reveals nuchal rigidity, aphasia, dysphasia, along with the patient having episodes of vomiting. What is your diagnosis?
A. Pneumothorax
B. Pneumocephalus
C. Neurogenic shock
D. Hypercapnia
- B: Pneumocephalus is the presence of air or gas within the cranial cavity. It is usually associated with disruption of the skull: after head and facial trauma, tumors of the skull base, after neurosurgery, or with scuba diving (rare). The CT scan of patients with a tension pneumocephalus typically show air that compresses the frontal lobes of the brain, which results in a tented appearance of the brain in the skull known as the Mount Fuji sign. The name is derived from the resemblance of the brain to Mount Fuji in Japan, a volcano known for its symmetrical cone. The presenting symptoms of pneumocephalus vary widely, but headache is almost always present. Experience with diagnostic pneumocephalus has shown that the headache is not induced by the intracranial air alone but that the dura mater must be stretched for pain to occur. Nausea, vomiting, vertigo, nuchal rigidity, aphasia, dysphasia, hemiplegia, and obtundation have all been associated with pneumocephalus, yet all are nonspecific symptoms. Treatment options for pneumocephalus vary. In some cases, the condition resolves on its own with some watchful waiting, application of oxygen, and surgery if not resolving in a timely fashion.
- Calculate the following patient’s cerebral perfusion pressure (CPP): BP 150/75, HR 140, RR 28, SpO2 100%, CVP 2, ICP 25.
A. 98
B. 125
C. 65
D. 75
- D: MAP = [(75 × 2) + 150] divided by 3 = 100. CPP = 100-25 = 75 mmHg
- You are transporting a normotensive patient, who is presenting with a history of head injury and complaining of extreme thirst. Your assessment reveals he is excreting large amounts of diluted urine, sunken appearance to the eyes, dry mouth, and tachycardia is noted. The initial treatment of the patient would be?
A. Restrict fluids
B. Administer Sandostatin
C. Aggressive fluid replacement and vasopressin
D. Administer anti-thyroid medication
- C: Diabetes insipidus (DI) is a condition characterized by excessive thirst and excretion of large amounts of severely diluted urine, with reduction of fluid intake having no effect on the latter. There are several different types of DI, each with a different cause. The most common type in humans is central DI, caused by a deficiency of arginine vasopressin (AVP), also known as antidiuretic hormone (ADH). The regulation of urine production occurs in the hypothalamus, which produces ADH. The hormone is stored for later release in the posterior lobe of the pituitary gland. The cause of central diabetes insipidus is usually damage to the pituitary gland or hypothalamus, most commonly due to surgery, a tumor, illness (such as meningitis), inflammation or a head injury. In some cases the cause is unknown. This damage disrupts the normal production, storage, and release of ADH.
- Cushing’s triad includes all of the following, except
A. Varying respiratory patterns
B. Narrowing pulse pressure
C. Widening pulse pressure
D. Bradycardia
- B: Cushing’s triad is defined as a widening pulse pressure (rising systolic, declining diastolic), change in respiratory pattern (irregular respirations), and bradycardia. It is sign of increased ICP, and it occurs as a result of the Cushing reflex. The body’s compensatory mechanism and response to decreased cardiac output is to stimulate the sympathetic nervous system. This will cause vasoconstriction and results in a rise in the diastolic pressure, causing a narrowed pulse pressure. A narrow pulse pressure, which is the difference between the systolic and the diastolic, is an early indication of shock. Look for hypovolemia or decreased cardiac output. A narrowing pulse pressure in shock is consistent with hypovolemic and cardiogenic causes. Septic shock will cause a widened pulse pressure. One way to differentiate shock in your patients is to look at the pulse pressure. A narrowing pulse pressure associated with hypovolemia would be hypovolemic. A narrowing pulse pressure associated with volume overload would be cardiogenic. A widening pulse pressure associated with hypovolemia would be septic. 27. D: The classic symptoms include
- A patient presenting with an initial loss of consciousness with a period of a lucid interval, with return of a normal neurologic status, suddenly complains of a headache, with a deteriorating level of consciousness. The patient is most likely experiencing a
A. Subdural bleed
B. Subarachnoid bleed
C. Intracerebral bleed
D. Epidural bleed
- D: The classic symptoms include transient loss of consciousness, recovery with a lucid interval during which the patient’s neurologic status returns to normal, and the secondary onset of headache and a decreasing level of consciousness. In children, bradycardia and early papilledema (optic disc swelling) may be the only warning signs. Epidural hematomas are usually caused by tears in arteries, resulting in a buildup of blood between the dura and the skull. The dura mater also covers the spine, so epidural bleeds may also occur in the spinal column. Often due to trauma, the condition is potentially deadly because the buildup of blood may increase pressure in the intracranial space and compress delicate brain tissue. Epidural hematoma commonly results from a blow to the side of the head. The pterion region which overlies the middle meningeal artery is relatively weak and prone to injury. Epidural hematomas are classified as acute or subacute. An acute epidural hematoma that is arterial in origin generally produces symptoms within a few hours. Subacute epidural hematomas are venous in origin and take a longer time to produce symptoms. These hematomas are associated with linear skull fractures in 90% of patients. Hemorrhages commonly result from acceleration-deceleration trauma and transverse forces (10% of epidural bleeds may be venous). Venous epidural bleeds are usually due to shearing injury from rotational or linear forces, caused when tissues of different densities slide over one another. Subdural hematoma is a collection of blood within the outermost meningeal layer, between the dura mater, which adheres to the skull, and the arachnoid mater enveloping the brain. Usually resulting from tears in veins that cross the subdural space, subdural hemorrhages may cause an increase in ICP, which can cause compression of and damage to delicate brain tissue. Subdural hematomas are classified as acute (within 24 hours), subacute (between 2-10 days), and chronic (after 2 weeks). Subdural hematomas are often life-threatening when acute, but chronic subdural hematomas are usually not deadly if treated. Elderly patients may have larger subdural hematomas, with slowly developing symptoms because they have larger potential subdural spaces as a result of cerebral atrophy. Subdural hematomas generally occur in children less than two years of age. Signs and symptoms include a bulging fontanelle and a large head (because of separation of the sutures) and retinal hemorrhages as a result of increased ICP.
- Brudzinski’s clinical sign may indicate
A. Subarachnoid bleed or meningitis
B. Subdural bleed or meningitis
C. Epidural bleed or meningitis
D. Basilar skull fracture
- A: Subarachnoid hemorrhage is bleeding into the subarachnoid space, the area between the arachnoid membrane and the pia mater surrounding the brain. This may occur spontaneously, usually from a ruptured cerebral aneurysm, or may result from head injury. Signs and symptoms can include a severe headache with a rapid onset (“thunderclap headache,” which is described as the worst ever), vomiting, neck stiffness (Brudzinski’s sign—severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed.), confusion, or a lowered level of consciousness, and sometimes seizures (1 in 14 patients). Intracerebral hemorrhage is a subtype of intracranial hemorrhage, which occurs within the brain tissue and not outside of it. Most intracerebral hematomas are found the frontal and temporal lobes, usually very deep, and are associated with necrosis and hemorrhage. The clinical picture may vary from no neurologic defect to deep coma. Intracerebral bleeds are the second most common cause of stroke, accounting for 30-60% of hospital admissions for stroke. High blood pressure raises the risk of spontaneous intracerebral hemorrhage by two to six times. More common in adults than in children, intraparenchymal bleeds due to trauma are usually due to penetrating head trauma but can also be due to depressed skull fractures; some may experience intense headaches. They may also go in to a coma before the bleed is noticed. A hit in the head or a fracture in the skull may also cause this bleed, acceleration-deceleration trauma, rupture of an aneurysm or arteriovenous malformation (AVM), and bleeding within a tumor.
- The presence of a Babinski’s sign in an adult patient would exhibited by
A. Flaccid movement of the toes
B. Plantar flexor reflex
C. Plantar extensor reflex
D. Toes fanning upward
- B: The Babinski’s sign can indicate upper motor neuron lesion constituting damage to the corticospinal tract (central nervous system). A normal Babinski’s reflex is plantar flexor (toes curl in “claw”) and an abnormal reflex is plantar extensor (toes fan out). In infants, the primitive reflexes are still present and will show an extensor reflex response. This happens because the corticospinal pathways that run from the brain down the spinal cord are not fully myelinated at this age, so the reflex is not inhibited by the cerebral cortex. The extensor response disappears and gives way to the flexor response around 12-24 months of age.
- You have been requested to transport a thirty-two-year-old male intravenous drug user who was brought to the ED without vascular access with a history of having had a witnessed generalized tonic-clonic seizure ten minutes prior to your arrival. The patient arrived post-ictal, but responsive. No other medical history was available. On examining, the blood pressure is130/80 mmHg, HR 88, respirations 14, and oxygen saturation of 98% on room air. The head is atraumatic, the pupils are 4 mm and reactive, cardiopulmonary exam was normal. Neurologically the patient is oriented to person only; he has no facial asymmetry, moves all four extremities, deep tendon reflexes were + 4 symmetrically, and no Babinski reflexes were present. The blood sugar is 110 mEq/dL. While looking for venous access over the patient’s scarred extremities, the patient began a second generalized tonic-clonic seizure. What is the “best” first line therapy for acute seizure management?
A. Phenytoin
B. Phenobarbital
C. Fosphenytoin
D. Benzodiazepines
- D: Seizure types are organized according to whether the source of the seizure within the brain is localized (partial or focal onset seizures) or distributed (generalized seizures). Partial seizures are further divided on the extent to which consciousness is affected (simple partial seizures and complex partial seizures). If consciousness is unaffected, then it is a simple partial seizure; otherwise, it is a complex partial seizure. A partial seizure may spread within the brain—a process known as secondary generalization. Generalized seizures are divided according to the effect on the body, but all involve loss of consciousness. These include absence, myoclonic, clonic, tonic, tonic-clonic, and atonic seizures. A mixed seizure is defined as the existence of both generalized and partial seizures in the same patient. Generalized epilepsy leading to status epilepticus is mostly seen in the acute state in one of the two situations: with generalized encephalopathy, including that immediately following trauma, and in patients who are known epileptics, who have reduced drug intake, and whose blood levels have fallen below therapeutic concentrations. Use a benzodiazepine as the first-line therapy. Seizure management requires a risk benefit analysis that balances the patient’s needs with the urgency of the situation. Lorazepam is the preferred first-line agent for seizure control due to its long-lasting anticonvulsant properties. Diazepam is equally effective but requires that a concomitant, long-acting antiseizure medication be administered, such as Dilantin. When the IV access is unavailable, alternate routes such as IM injections of Midazolam, rectal solutions of Diazepam, and IM Fosphenytoin should be considered; of the three, IM Midazolam is probably the fastest and easiest to use. Alternative agents that have been used to manage seizure activity include Phenobarbital, Lidocaine, etomidate, propofol, and Paraldehyde.
- Which cranial nerve is affected with a patient presenting with Bell’s Palsy?
A. I
B. V
C. VII
D. X
- C: The facial nerve is the seventh (VII) of twelve paired cranial nerves. It emerges from the brainstem between the pons and the medulla, controls the muscles of facial expression, and functions in the conveyance of taste sensations from the anterior two-thirds of the tongue and oral cavity. It also supplies preganglionic parasympathetic fibers to several head and neck ganglia. Patients may suffer from acute facial nerve paralysis, which is usually manifested by facial paralysis. Bell’s palsy is one type of idiopathic acute facial nerve paralysis, which is more accurately described as a multiple cranial nerve ganglionitis that involves the facial nerve, and most likely results from viral infection and also sometimes as a result of Lyme disease. Voluntary facial movements, such as wrinkling the brow, showing teeth, frowning, closing the eyes tightly (inability to do so is called lagophthalmos), pursing the lips, and puffing out the cheeks, all test the facial nerve.
- Cranial nerve III is also known as the
A. Optic nerve
B. Oculomotor nerve
C. Olfactory nerve
D. Auditory nerve
- B: Cranial nerve III, which is the oculomotor nerve, innervates five intrinsic eye muscles: levator palpebrae superioris, superior rectus, medial rectus, inferior rectus, and inferior oblique, which collectively perform most eye movements. It also sends parasympathetic efferents (via the ciliary ganglion) to the muscles controlling pupillary constriction and accommodation. The motor fibers originate in the oculomotor nuclei of the midbrain.
- You are transporting a twenty-six-year-old male patient involved in a fall injury. Upon your arrival on the scene, your assessment reveals an awake patient who is not able to shrug his shoulders. Which cranial nerve is most likely affected?
A. III
B. VII
C. X
D. XI
- D: Cranial nerve VI, which is the accessory nerve (spinal accessory nerve), originates from neurons in the medulla and in the cervical spinal cord. It has a cranial root, which joins the vagus (cranial nerve X) nerve and sends motor fibers to the muscles of the larynx, and a spinal root, which sends motor fibers to the trapezius and the sternocleidomastoid muscles. Damage to the nerve produces weakness in head rotation and shoulder elevation.
- A patient diagnosed with Guillan-Barre would most likely present with all of the following, except
A. Descending paralysis
B. Ascending paralysis
C. Dysphagia
D. Dysesthesia
- A: Guillain-Barre syndrome is an acute inflammatory demyelinating polyneuropathy (AIDP), an autoimmune disorder affecting the peripheral nervous system, usually triggered by an acute infectious process. It is frequently severe and usually exhibits as an ascending paralysis noted by weakness in the legs that spreads to the upper limbs and the face, along with complete loss of deep tendon reflexes. With prompt treatment by plasmapheresis or intravenous immunoglobulins and supportive care, majority of patients will regain full functional capacity. Myasthenia gravis is an autoimmune neuromuscular disease, leading to fluctuating muscle weakness and fatiguability. It is an autoimmune disorder, in which weakness is caused by circulating antibodies that block acetylcholine receptors at the postsynaptic neuromuscular junction, inhibiting the stimulative effect of the neurotransmitter acetylcholine. Myasthenia is treated medically with cholinesterase inhibitors or immunosuppressants, and, in selected cases, thymectomy. Symptoms, which vary in type and severity, may include asymmetrical ptosis (a drooping of one or both eyelids), diplopia (double vision) due to weakness of the muscles that control eye movements, an unstable or waddling gait, weakness in arms, hands, fingers, legs, and neck, a change in facial expression, dysphagia (difficulty in swallowing), shortness of breath and dysarthria (impaired speech, often nasal due to weakness of the velar muscles). In myasthenic crisis a paralysis of the respiratory muscles occurs, necessitating assisted ventilation to sustain life. In patients whose respiratory muscles are already weak, crises may be triggered by infection, fever, an adverse reaction to medication, or emotional stress. Diagnostic testing is done by injecting the drug edrophonium chloride (Tensilon, Reversol) or neostigmine (Prostigmin) into a vein and watching for rapid improvement of strength, usually of eye muscles. In patients with myasthenia gravis, involving the eye muscles, Edrophonium Chloride will briefly relieve eye muscle weakness. Improvement in strength of speech may also be considered a positive test.
- You are transporting a twenty-five-year-old male with a history of acute alcohol intoxication who was involved in a single vehicle roll-over two hours prior to your arrival. The patient is presenting with variable loss of motor function and sensory function from the nipple line down. Which dermatome would most likely be affected and what clinical condition you do suspect?
A. C3; central cord syndrome
B. C6; Brown-séquard syndrome
C. T4; anterior cord syndrome
D. T10; anterior cord syndrome
- C: Central Cord syndrome is a type of injury that usually results from hyperextension and is characterized by a disproportionally greater motor impairment of the upper than the lower extremities with variable sensory loss below the level of injury. Sacral sparing typically occurs. Two very important determinants of an incomplete, as opposed to a complete, lesion of the spinal cord are preservation of voluntary rectal sphincter tone and perianal sensation (“sacral sparing”). To check for voluntary rectal sphincter tone, insert a gloved finger in the rectum and request the patient, if cooperative, to squeeze down as if attempting to prevent movement of the bowels. If able to do so, there is substantial indication of an incomplete, as opposed to a complete, spinal cord injury, i.e., some spinal neural pathways are intact.
- You have been requested to transport a twenty-year-old male involved in a motor vehicle accident. Your assessment reveals an ethanol-like odor on his breath, GCS 15, with slurred speech, and the patient is able to grossly flex the arms at the elbow but unable to extend his arms at the elbows or wrists or flex or extend the fingers, with no sensation to the medial side of the arm and small finger. The patient was noted to have the capability of extending both lower legs at the knee, but definite weakness was present. He was able to extend and flex his ankles and toes. The clinical findings affect which dermatome and what clinical condition is suspected?
A. C5; anterior cord syndrome
B. C6; central cord syndrome
C. C8, T1; central cord syndrome
D. T4; Brown-séquard syndrome
- A: The presence of the plantar extensor reflex (toes fan upward) in an adult patient can indicate damage to the nerve pathways connecting the spinal cord and brain. It is wrong to say that the Babinski’s reflex is positive or negative; it is present (plantar extensor reflex—toes fan upward which is bad) or absent (plantar flexor response—toes curl downward which is good).
- The presence of a plantar extensor reflex in an adult patient can indicate
A. Damage to nerve pathways connecting the spinal cord and brain
B. Intact motor neuron function
C. Damage to the nerves in the lower extremities
D. Increased ICP
- C: The absence of doll’s eye sign indicates injury to the midbrain or pons, involving cranial nerves III and VI. It typically accompanies coma caused by lesions of the cerebellum and brain stem. This sign usually can’t be relied upon in a conscious patient because he can control eye movements voluntarily. Absent doll’s eye sign is necessary for a diagnosis of brain death.
- Oculocephalic reflex is also known as
A. Babinski
B. Cold caloric
C. Doll’s eyes
D. Consensual reflex
An indicator of brainstem dysfunction, the absence of the doll’s eye sign is detected by rapid, gentle turning of the patient’s head from side to side. The eyes remain fixed in midposition, instead of the normal response of moving laterally toward the side opposite the direction the head is turned. Lopez, Orchid Lee (2011-02-15). Back To Basics: Critical Care Transport Certification Review (p. 211). Xlibris. Kindle Edition.
- The oculovestibular reflex exam is used to assess
A. The presence of ICP
B. Brainstem function
C. Spinal cord injury
D. Pupil response
- B: Clinical evaluation of brain death can be performed with the application of the oculovestibular reflex (cold-caloric exam). With head on bed at 30 degrees, instill 50 mL of iced water into ear canal. A normal response (presence of oculovestibular reflex) is tonic deviation of the eyes toward the irrigated ear.
- Mydriasis is defined as
A. Increased salivation
B. Pinpoint pupils
C. Dilated pupils
D. Fixed, midposition pupils
- C: Mydriasis is an excessive dilation of the pupil due to disease, trauma, or the use of drugs. A mydriatic pupil will remain excessively large even in a bright environment and is sometimes referred to as “blown pupil.” Pupillary dilation (mydriasis) indicates unopposed sympathetic activity due to impaired parasympathetic axons. This may reflect compression or distortion of the oculomotor nerve (CN III) by either primary injury or herniation. Mydriasis also may be an effect of adrenergic stimuli, such as epinephrine, anticholinergics, cocaine, PCP, and drug withdrawal. The classic fixed and dilated “blown pupil” is a unilateral phenomenon that may occur when a rapidly expanding intracranial mass, including blood from a hemorrhage, is compressing cranial nerve III. It may also represent herniation of the uncus of the temporal lobe. The opposite, constriction of the pupil, is referred to as miosis.
- The patient presenting with Battle’s and Racoon’s clinical signs is most likely experiencing which of the following?
A. Epidural bleed
B. Basilar skull fracture
C. Subdural bleed
D. Increased ICP
- B: A basilar skull fracture (or basal skull fracture) is a fracture of the base of the skull, typically involving the temporal bone, occipital bone, sphenoid bone, and/or ethmoid bone. This type of fracture is rare, occurring as the only fracture in just 4% of severe head injury patients. Such fractures can cause tears in the membranes surrounding the brain, or meninges, with resultant leakage of the cerebrospinal fluid (CSF). The leaking fluid may accumulate in the middle ear space and dribble out through a perforated eardrum (CSF otorrhea) or into the nasopharynx via the eustachian tube, causing a salty taste. CSF may also drip from the nose (CSF rhinorrhea) in fractures of the anterior skull base, yielding a halo sign. Clinical signs include Battle’s sign, which is ecchymosis of the mastoid process of the temporal bone and Raccoon eyes is periorbital ecchymosis (“black eyes”).
- Which of the following is most likely affected with a patient presenting with an epidural bleed?
A. Middle meningeal artery
B. Carotid artery
C. Communicating artery
D. Subclavian artery
- A: Epidural hematomas are usually caused by tears in arteries, resulting in a buildup of blood between the dura and the skull. The middle meningeal artery runs in a groove on the inside of the cranium beneath the pterion, which is vulnerable to injury at this point, where the skull is thin. A blow or fracture of the temporal bone is often the cause of a rupture of the middle meningeal artery, which may cause an epidural hematoma.
- Another term used to describe pinpoint pupils is
A. Mydriasis
B. Miosis
C. Mitosis
D. Doll’s eyes
- B: The opposite of mydriasis (dilated pupil) is constriction of the pupil and is referred to as miosis when less than or equal to two millimeters. This is a normal response to an increase in light but can also be associated with certain pathological conditions, microwave radiation exposure, and certain drugs, especially opioids.
- You would expect the normal range when measuring a mean arterial pressure (MAP) to be
A. 50-60 mmHg
B. 70-90 mmHg
C. 80-100 mmHg
D. 100-120 mmHg
- C: Normal MAP is 80-100 mmHg.
- Which clinical sign/symptom initially would indicate that a ventricular-peritoneal shunt is malfunctioning?
A. Deteriorating level of consciousness
B. Vomiting
C. Hypotension
D. Bradycardia
- B: The best treatment for hydrocephalus is the placement of an extracranial shunt from the ventricles to an outside absorptive surface such as ventriculoperitoneal, ventriculoatrial, or ventriculopleural. Shunts usually consist of three parts: a. Proximal end that is radiopaque and is placed into the ventricle. This end has multiple small perforations. b. Valve—this allows for unidirectional flow. Can adjust various opening pressures. Usually has a reservoir that allows for checking shunt pressure and sampling CSF. c. Distal end that is placed into the peritoneum or another absorptive surface by tracking the tubing subcutaneously.