Senior Report 7.6

Case Presentation by Dr. Meredith Hill-Ciesielski, MD

CHIEF COMPLAINT(S): “Not acting right”

HISTORY OF PRESENT ILLNESS: This is a 68-year-old male who was sent in for a change in mental status.  The patient’s daughter went to visit her father.  When she arrived to the house her mom said he was not responding appropriately.  The daughter tried to get the patient up off the couch to take him to the hospital but he was unable to get out of the chair. He was also noted to have slurred speech.  When he arrived in the emergency department, he was unable to provide any history and was made a medical code.

REVIEW OF SYSTEMS:

Could not be obtained secondary to patient’s condition

PMH: Hypertension; otherwise unknown
Surg HX: Unknown
Medications: Maxzide 25 mg/37.5 mg, losartan 100 mg, other medications unsure
Allergies: The daughter believes he is not allergic to any medications
Social Hx: No drug use per family

PMD: He has a doctor but the daughter does not know his/her name

EXAMINATION OF ORGAN SYSTEMS/BODY AREAS:
Vitals: Temperature was 36.3 C, HR 74 bpm, RR 12/m, blood pressure 166/86 mmHg, SpO2 100% on room air.  Weight 100kg
Capillary blood glucose:125 mg/dL
General: Patient’s eyes closed half way, moaned as he was transferred over to the stretcher.  No acute respiratory distress noted.
HEENT: pupils were pin point, not reactive to light. No pallor, mucous membranes moist. Patient had a weak gag on arrival
Neck: Supple, no rigidity
Resp: Normal respiratory effort with a slightly slow respiratory rate, clear on inspiration and expiration
Heart: Regular rate and rhythm, and no murmur or gallop. Pulses were intact and symmetrical
Abdomen: Soft, nontender, nondistended
Musculoskeletal: Distal pulses decreased but present. There is no clubbing or cyanosis
Skin: No rashes
Neurological: Patient was very sleepy, his eyes were closed but he would open to verbal stimuli. He would follow simple commands such as squeezing fingers.  He was able to lift arms off bed against gravity but had generalized weakness. His tongue protruded midline. Speech was unintelligible. Strength was 4/5 grip strength bilaterally. He could lift both legs and arms off the table but only for about one to 2 seconds; not sustainable.  He had no clonus.  He was very sleepy but when stimulated, he would attempt to try to follow commands

Questions:

1. After placing the patient on a cardiac monitor, establishing IV access and obtaining a normal cbg (which was all done for patient) what would be your next step of action?

  1. Administer 0.2mg naloxne to patient
  2. Obtain blood cultures and give Ceftriaxone, Vancomycin and Acycolvir
  3. Send the patient for a CT head without contrast
  4. Adminsiter 500mg IM thiamine and send the patient to TCU for sobriety

2. While you are evaluating the patient you note that his respirations become more shallow and he is no longer responsive to pain nor verbal stimuli.  His head rolls back on the stretcher and his eyes close.  What is next step of action?

  1. Naloxone 0.2mg IV
  2. Shake the patient harder because he just may have overdosed on his clonidine
  3. Intubate the patient using RSI
  4. Send the Patient for a CT head without contrast

3. Assuming this patient does have a stroke syndrome, what/where is the most likely etiology?

  1. Basilar artery occlusion
  2. Dolichoectasia of the Vertebral artery
  3. Posterior inferior cerebellar artery (PICA) occlusion
  4. Posterior cerebral artery occlusion (PCA)

4. Patient returns from CT which does not show any acute intracranial hemorrhage.  His neurological status and exam is unchanged. You have consulted neurology and they feel the patient is a good tPa candidate.  What is your next course of action?

  1. Do not give tPa because the patient’s blood pressure is too high.
  2. Give the patient 9mg dose of tPa then infuse 80mg over the next hour
  3. Give the patient 90mg bolus of tPa then repeat the CT head
  4. Do not give tPa because the patient is too old.
  5. Do not give tPa because the patient is not having a stroke

 

Answers & Discussion:

Question 1 answers: 3, 1 (either one of these counted as the correct answer)
Explanation:

This patient’s exam and history are consistent with a possible stroke so obtaining a CT head would be a priority however, given that he was rather sedated and had pin point pupils, trying a small dose of naloxone prior to CT would not be a bad decision (naloxone is really only given to help with respiratory effort rather than wake them up, per se).  In a situation where the patient appears to have an acute onset of weakness and altered mental status with hard neurological abnormalities on exam, assuming alcohol intoxication would be disastrous. Working up and treating for meningitis is a consideration; however, there are few signs and symptoms on history and examination that would point you primarily to this disease process. The current American Heart Association and American Stroke Association recommend that a protocol be in place to expedite noncontrast CT scans for any potential stroke cases and have Pt/INR/aPTT drawn upon arrival so that treatment goals can be decided within 60 minutes.  The goal at our institution is 45 minutes from door to PT/INR/aPTT and 15 minutes from door to CT scan so that time can be allowed for lab processing and reading the CT as well as evaluation by the stroke team. CT head without contrast is the preferred first image modality because you are ruling out hemorrhage, tumor, abscess and stroke mimics.

Question 2 answer: 3
Explanation:

Ensuring an adequate airway is a must.  This patient lost the ability to protect his airway and should not be allowed to go to CT scan without being intubated.  Although not altogether inappropriate, a repeat dose of naloxone is unlikely to be of benefit after decompensating so quickly after the initial dose. Alternative diagnoses should be considered.  Clonidine can present in a similar manner to opioids; regardless, you would still want to protect the airway.

Question 3 answer: 1
Explanation:

This patient’s presentation is most consistent with a basilar artery occlusion. Typical findings of a basilar artery occlusion include: coma, quadrapeggia, and “Locked in Syndrome”. Locked in Syndrome Where the patient has complete paralysis with upward gaze.  Patient’s often present initially with unilateral weakness but may still show some weakness on the unaffected side.  Patients can have incoordination of limb movements and gait ataxia. You can see jerking or shaking often misdiagnosed as seizure. Patient’s can completely lose their ability to speak but will be able to open their mouths and stick out their tongue. Pooling secreation are a problem which is why airway management is critical here. Oculomotor symptoms are common so expect eye deviation or small pupils, ie this patient had pin point pupils.  Sensory deficits are usually not as common. Altered level of consciousness is also common. These types of stroke have higher mortality and poorer outcomes.

Dolichoestasia is elogation, widening and tortuosity of the artery.  Usually affects the verebral and basilar arteries. Usually the artery has a large external diameter and a thisn arterial wall. As the artery stretches and become more tortuous, the flow decrases resulting in a stroke like syndrome. As the artery dilates it can compress surrounding structures and cause symptoms or the artery can rupture which would lead to a catastrophic outcome.  Basically this patient’s symptoms are more consistent with a basilar artery stroke then verebral. Vertebral artery occulsion would present with symptoms of vertigo, nausea, vomiting and unilateral Horner’s syndrome and less likely a sedated state. Which is why this answer is less likely.

Posterior inferior cerebellar artery occlusion can cause a headache usually at the occiput. Patients have vomiting, gait ataxia, truncal ataxia and limb incoordination.  Patient will have abnomal cerebellar testing.  If the infarction in limited to the vermis, patients can have vertigo and nystagmus. Patients will also feel they are being pulled to the ipsilateral side. Ipsilateral facial pain (CN V), vertigo (vestibular nucleus), headache, Horner syndrome (descending sympathetic tract), dysphagia and dysphonia (CN IX and X), and ipsilateral loss of pain and temperature (spinothalamic tract). Wallenberg Syndrome is a neurological condition caused by stroke in vertebral or PICA.  Symptoms include dysphagia, hoarse voice, dizziness, nausea and vomiting, nystagmus, and ataxia.

Posterior Cerebral Artery Infarction typically presents with patients having visual field deficits (contralateral homonymous hemianopsia) and most commonly a unilateral headache.  Light touch deficits, loss of ability to read without agraphia, memory loss, unilateral 3rd nerve palsy, and minimal motor function loss.

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Question 4 answer: 2
Explanation:

Recombinant Tissue Plasminogen Activator (rtPA) is currently a very hot topic. Regardless, having made the diagnosis of basilar artery occlusion and stroke, he does meet criteria for administration.

Indications for rtPa:

  • -Measurable diagnosis of acute ischemic stroke: use of NIHSS is recommended. Symptoms should not be clearing, minor, or isolated.  Caution advised for giving tPa to patients with severe stroke (NIHSS>22)
  • -Age greater than of equal to 18
  • -Time of onset of symptoms less than or equal to 3 hours.

Exclusion:

  • -symptoms consistent with SAH
  • -seizure with postictal residual neurological impairments
  • -previous head trauma or stroke in last 3 months
  • -previous MI in last 3 months
  • -previous GI or urinary tract hemorrhage in last 21 days
  • -major surgery within 14 days
  • -prior intracranial hemorrhage
  • -pretreatment systomlic BP>185 or diastolic>110 despite therapy given
  • -Evidence of active bleeding or acute fracture
  • -blood glucose<50
  • -INR>1.7
  • -use of heparin within preceding 48 hrs and a prolonged aPTT
  • -platelets count<100,000
  • -CT head shows multilobar infarction (hypodensity more than 1/3 cerebral hemisphere) hemorrhage or tumor
  • -failure of patient’s responsible party to understand risks, benefits, and alternatives to treatment with tPA after full discussion

 

Dosing of tPA:
The total dose of rtPA is 0.9mg/kg. With a max dose of 90mg. 10% given as a bolus then the rest given over 60 minutes. BP and neuro checks should be preformed every 15 minutes during for the first 2 hours after starting the infusion.

This patient did receive rtPA and then went for a confirmatory CT angiogram which was suspicious for a basilar artery thrombus. A confirmatory angiogram demonstrated diffuse atherosclerotic disease and critical stenosis of the basilar artery. His neurological examination improved remarkably and he was able to walk and talk upon discharge to home.  He elected to do physical therapy as an outpatient.

Sources:

Caplan, et al. Posterior Circulation Cerebrovascular Syndromes. Oct 6 2013. Up to Date

Tintinalli’s Emergency Medicine 3rd ed.

http://www.csuchico.edu/~pmccaffrey//syllabi/CMSD%20320/362unit11.html

http://en.wikipedia.org/wiki/Anatomy_of_the_cerebellum

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