Neurovascular Emergencies

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Neurovascular Emergencies

• Victor Politi, M.D., FACP
• Medical Director, SVCMC, School of Allied Health,
  Physician Assistant Program

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Anatomy

• Skull
• closed system/ unable to expand
• Brain- 3 parts
• cerebellum
• cerebrum
• brain stem
• Spinal column
• Nerves

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Anatomy

• Cerebrum
• controls higher mental function personality,
  memory, reason, senses
• Cerebellum
• small posterior portion of brain coordinates
  muscle movements and balance
• Brainstem
• top of the spinal cord, base of the brain
  controls vital functions like heart rate,
  breathing, gag reflex

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Anatomy

• Meninges-
• the covering around the brain and spinal cord
• Three layers
• dura mater
• arachnoid
• pia mater

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Anatomy

• Cerebrospinal fluid
• fluid that cushions the brain and spine and helps
  circulate nutrients
• Spinal cord
• Attached to brainstem and carries information
  between the body and brain

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Neurological Changes

• Neurological changes come from
• Hypoxia
• Pressure

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Brain Injury - Hypoxia

• Ischemia
• mismatch between needed cerebral blood flow and
  the amount of perfusion supplied
• Injury
• After a period of ischemia, the brain becomes
  damaged
• Infarction
• Irreversible death of brain tissue

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Neurological Changes

• Reasons for increased ICP (pressure)
• Bleeding
• Edema
• Inflammation
• Tumor

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Neurological Changes - Bleeding

• Bleeding
• aneurysm
• trauma
• CVA
• subdural (SDH) - bleeding below the Dura
• Epidural- bleeding above the Dura
• Subarachnoid (SAH)
• Intracerebral- bleeding within the brain

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Neurological Changes-EDEMA

• Edema -
• general swelling of brain tissue in response to
• trauma (injury)
• hypoxia (cellular death)

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Neurological Changes -

• Inflammation -
• infection of brain tissue
• Tumor -
• cancer
• arteriovenous malformation (AVM)

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Assessment of Neurological Function

• Level of consciousness
• Glasgow Coma Scale (GCS) the standard measure
  used to quantify level of consciousness in head
  injury patients
• Widely used in scoring systems, treatment
  protocols and general clinical decision-making in
  critically ill patients

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Glasgow Coma Score

• The GCS is scored between 3 and 15, 3 being the
  worst, 15 the best
• GCS is composed of 3 parameters Best Eye
  Response, Best Verbal Response, Best Motor
  Response
• A GCS of 13 or higher correlates with a mild
  brain injury, 9-12 is moderate injury and 8 or
  less a severe brain injury

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Glasgow Coma Scale

• E (eye) M (motor) V (verbal) 3 to 15
• 90 less than or equal to 8 are in coma
• Greater than or equal to 9 not in coma
• 8 is the critical score
• Less than or equal to 8 at 6 hours - 50 die
• 9-11 moderate severity
• Greater than or equal to 12 minor injury
• Coma is defined as (1) not opening eyes, (2) not
  obeying commands, and (3) not uttering
  understandable words.

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Glasgow Coma Scale (GCS)

• Measures best response
• Eyes scaled 1-4
• Verbal scaled 1-5
• Motor scaled 1-6
• Total 3-15

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Glasgow Coma Scale (GCS)- Eyes
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Glasgow Coma Scale (GCS)-Verbal
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Glasgow Coma Scale (GCS)-Motor
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Assessment of Neurological FunctionDecorticate
Posturing

• Seen when there is lesion of corticospinal tract
  superior to level of brainstem
• indicated in comatose patient who responds to
  sternal rub by full flexion of the elbows,
  wrists, fingers, as well as plantar flexion of
  feet with extension and internal rotation of legs

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Assessment of Neurological Function - Decerebrate
posturing

• Seen in patients with lesions of brainstem
• patients exhibit extension of the arms, flexion
  of the wrists, jaw-clenching, back-arching,
  plantar flexion, neck extension, either
  spontaneously or in response to sternal rub

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Assessment of Neurological Function -Disability

• Severe headache
• Confusion, disorientation, memory loss
• Abnormal or slurred speech
• Loss of vision or partial vision (one or both
  eyes)
• Poor balance or lack of coordination
• Seizures
• Nausea/emesis

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Assessment of Neurological Function -Disability

• Numbness, weakness, clumsiness or paralysis of an
  arm, leg or side of the face

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Cushing Triad

• Increased BP Decreased HR
• Irregular Respirations

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Cushing Triad

• Increase in BP to overcome the increase of
  pressure inside the skull
• Brain trying to prevent infarct
• Decreased HR to allow the heart to pump more
  effectively and increase BP
• Cheyne-Stokes respirations to try to blow off CO2
• CO2 is a potent vasodilator

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Cushing Triad

• CO2 is a potent vasodilator
• Increase of CO2 in the blood
• Causes increase in blood volume intracranially
• Decrease in CO2 in the blood
• Causes decrease in blood volume intracranially

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Cushing Triad

• The body may attempt to decrease ICP by reducing
  the blood volume in the skull
• this is done by regulating the respiratory rate

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Herniation

• The increased ICP is forcing the brain through
  the Foramen Magnum
• Signs and Symptoms
• worsening GCS
• sudden change in pupil response (dilation or no
  responsiveness)
• Change in VS indicating Cushing's response
• General demise of patient
• (generally all must be occurring)

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Herniation

• Suspected herniation is the only time it is
  acceptable to hyperventilate your patient

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Treatment

• Airway
• Increased ICP may diminish or paralyze the gag
  reflex
• - allowing aspiration
• Suction
• Positioning
• - C Spine ?

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Treatment

• Breathing
• severe brain injury may interfere with breathing
  center of the brain
• be ready to BVM patient if necessary
• High flow oxygen (10-15 lpm)

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Treatment

• Circulation
• Treat for shock
• prevent hypotension - hypoxia and infarct of
  brain tissue
• IV initiate
• assist with BP control
• med line if seizure

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Treatment

• Positioning
• What can be done to assist flow into the skull
• maintain blood pressure
• What can be done to assist flow out of the skull
• HOB elevated to 30
• C-collar removed

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Treatment

• Communicate with the patient
• whether they respond or not
• They may be awake and cannot communicate

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Neurovascular Emergencies

• TIA (transient ischemic attack)
• Stroke
• Hemorrhage
• Aneurysm
• Tumor
• Seizure
• Headache (worst of life)

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Headache
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Epidemiology

• 1-2 of visits to the emergency department
• 4 of visits to the physicians office
• Most have primary headache disorders
• Among all patients with headache in an ED, 1
  will have SAH
• In patients with the worst ever headache of their
  life, and normal neurological exam, 12 will
  have SAH

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Working classification of headache

• Migraine (10 prevalence)
• Tension-type headache(30-80 prevalence) (CTH-2)
• Other headache (includes cluster HA and secondary
  headaches)

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Secondary headache disorders

• Stroke, SAH
• Tumour
• Infection
• Systemic disorders- thyroid disease, HT,
  pheochromocytoma.
• Temporal arteritis
• Ophthalmological and ENT causes.
• Traumatic

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Danger signals

• First or worst headaches
• Headache on exertion, early morning, or nocturnal
• Progressive headache
• New onset headache in adult gt50 years old
• Abnormal physical or neurological findings
  (fever, stiff neck)

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History

• Past history of headaches
• first, worst, different, progressive,
  persistent
• Age of onset
• gt 50 years
• Headache characteristics
• Palliative
• Quality
• Region
• Severity (0-10)
• Timing

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History

• Associated Symptoms
• Fever/Chills/Nightsweats
• Nausea/Vomiting
• Photophobia Phonophobia
• Neck pain or stiffness
• Alterations in level of consciousness
• Focal neurologic symptoms
• Family History

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Physical Examination

• General Exam
• Vital Signs
• General Appearance
• HEENT (Trauma, dentition, sinus/temples)
• Neck (ROM, Kernigs and Brudzinskis sign)
• Skin (Rash, bruising, hemorrhages)
• Lymph Nodes

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Physical Examination

• Neurologic Exam
• Mental Status LOC, Orientation, Language,
  mood/thoughts
• Cranial Nerves
• I Not tested unless history suggestive
• II Reading VA each eye, VF by confrontation with
  double simultaneous stimulation, fundoscopy
• III, IV, VI Lateral and vertical eye mvts,
  pupillary light response
• V Pinprick and touch sensation on face
• VII Close eyes, show teeth
• VIII Whispered voice each ear
• IX, X Palate lifts in midline, gag present
• XI Shrug shoulders
• XII Protrude tongue

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Physical Examination

• Neurologic Exam (cont.)
• Limbs Each limb tested separately
• Tone
• Power of main muscle groups (0-5 MRC Scale)
• Coordination finger-to-nose, heel-to-shin
• Tendon reflexes
• Plantar response
• Pinprick and light touch on hands and feet
• Double simultaneous stimulation on hands and feet
• Joint position sense in hallux and index finger
• Vibration sense at ankle and index finger
• Gait
• Rombergs test

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Laboratory Studies

• Blood
• CBC
• Chemistry panel
• ESR
• PT/PTT (Consider hypercoagulable profile)
• TSH
• ABG (if clinically indicated)
• Drug screen
• Urinalysis

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Imaging

• X-rays
• CXR
• Cervical Spine X-ray
• Cranial computed tomography (CT)
• preferred initial imaging study for acute
  headache
• Cranial magnetic resonance imaging (MRI)
• Magnetic resonance angiography (MRA)
• Cerebral angiography

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Other Studies

• Lumbar puncture (LP)
• indicated if acute or chronic meningitis, SAH,
  pseudotumor cerebri (IIT) or low CSF pressure
  headache suspected
• preferable to perform CT before LP
• Electroencephalogram (EEG)
• indicated if seizures are suspect

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Differential Diagnosis

• Primary headache
• Migraine
• Tension-type headache
• Cluster headache
• Indomethacin-responsive headache syndromes
• Secondary headache

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Secondary Headache DDx

• Subarachnoid Hemorrhage (SAH)
• first or worst headache
• physicians consistently misdiagnose SAH
• pts with the greatest potential tx benefits are
  most often misdiagnosed
• early complications develop in patients with an
  incorrect dx
• Meningitis
• associated with fever, neck stiffness, confusion
  

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Secondary Headache DDx

• Subdural hematoma
• recent trauma (/-)
• Stroke (Ischemic or Hemorrhagic)
• occurs with focal neurologic sx
• Cervicocephalic arterial dissection
• trauma hx (/-), neck pain, ipsilateral Horners
• Giant cell arteritis
• gt 50 yrs, visual loss, temporal pain, ? ESR

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Secondary Headache DDx

• Dental abscesses/TMJ
• oral or jaw pain initially
• Sinusitis
• overdiagnosed, dx more likely with fever/purulent
  nasal discharge
• Trigeminal neuralgia
• sharp unilateral pain usually over maxillary
  distribution
• Low CSF pressure headache
• sx resolve in supine position and recur when
  upright
• Acute Glaucoma
• periorbital pain, conjuntival injection, lens
  clouding

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Subhyaloid hemorrhage
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Physical findings in SAH

• Nuchal rigidity
• Altered consciousness,
• Papilledema, retinal and subhyaloid hemorrhage,
  3rd and 6th nerve palsy,
• Bilateral leg weakness, abulia,
• Nystagmus, ataxia,
• Aphasia, hemiparesis, left-sided visual neglect

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Diagnosis of SAH

• 25-51 of patients receive an incorrect diagnosis
• 91 of those with correct diagnosis have a
  favorable outcome at 6 weeks Vs 53 with an
  incorrect diagnosis
• Median delay in diagnosis(4 studies) 3 - 14
  days

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Reasons for misdiagnosis of SAH

• Failure to appreciate the spectrum of clinical
  presentation
• Failure to understand the limitations of CT
• Failure to perform and correctly interpret the
  results of LP

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Indications for neuroimaging

• First or worst headache
• Progressive or CDH
• Side-locked headache
• Headaches not responding to treatment
• New onset headache in patients with cancer, HIV
  infection, or age gt50 yrs
• Associated fever, stiff neck, neurological
  deficits

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CT versus MRI

• Preferred in SAHICH

• Posterior fossa lesions
• CVT
• Meningeal disease
• Cerebritis and abscess
• Pituitary pathology

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SAH
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L.P in evaluation of headache

• Suspected SAH if CT is negative
• (Deterioration after LP in patients with clots
  on CT or a dilated pupil)
• Start antibiotics in patients with suspected
  meningitis, while waiting for CT
• CSF pressure should be measured
• Distinguish traumatic tap from true hemorrhage

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L.P in evaluation of headache

• First or worst headache - SAH, meningitis
• Headache with features s/o infection- meningitis
  /encephalitis
• CVT - elevated CSF opening pressure

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Probability of detecting xanthochromia in CSF
with spectrophotometry after SAH

• 12 hours 100
• 1 week 100
• 2 weeks 100
• 3 weeks gt70
• 4 weeks gt40

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Angiography

• In proven SAH- 4 vessel angio to identify source
  and r/o multiple aneurysms
• Initial arteriogram negative in up to 16 of SAH
• MRA detects 90 of saccular aneurysms of gt5mm
• Spiral CT angio detects 85 of saccular aneurysms

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Thunderclap headache

• Sudden severe headache with max intensity within
  1 minute
• Normal CT scan
• Normal CSF study
• 180 patients followed up for 1- 3 years. None
  developed SAH.
• Wijdicks 1988, Markus 1991, Linn 1994

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Thunderclap headache

• Primary causes- Migraine, benign thunderclap
  headache, benign orgasmic headache
• Secondary-unruptured saccular aneurysm, cerebral
  vasospasm, CVT, arterial dissection, pituitary
  apoplexy, occipital neuralgia
• Evans RW 2000

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Cerebral Aneurysm
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Cerebral aneurysm

• The brain has many arterial blood vessels that
  supply blood pumped by the heart. When the wall
  of a blood vessel becomes weak and/or thin, it
  forms a bulge or a bubble. This bulge or bubble
  is called an aneurysm.
• Aneurysms may also rupture, causing bleeding in
  the brain. This bleeding results in Subarachnoid
  Hemorrhage

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Symptoms

• Often asymptomatic
• Focal neurological deficits depending on
  location for example, if the aneurysm compresses
  the area of brain controlling the left leg, then
  left leg weakness will occur.
• Mild headaches
• Nausea
• Neck stiffness
• Severe "thunderclap" headaches if the aneurysm
  ruptures (Subarachnoid Hemorrhage)

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Causes

• Genetic predisposition in persons with polycystic
  kidney disease or coarctation of the aorta
• Cause often unknown

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Exam

• Focal neurological deficits
• Neck stiffness if aneurysm has ruptured

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Imaging

• Cerebral Angiography (dye is injected into the
  carotid artery to get an image of the blood
  vessels of the brain)
• CT scan will usually show bleeding after an
  aneurysmal rupture
• MRI

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Laboratory Studies

• Lumbar puncture (spinal tap) -- cerebrospinal
  fluid will show blood after an interval of time
  if there is aneurysm rupture.
• ECG- may cause EKG abnormalities
• Subarachnoid hemorrhage may cause heart
  abnormalities

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Treatment

• Unruptured aneurysms
• Large Aneurysms are surgically clipped at their
  bases to prevent rupture.
• Small (less than 1/2 centimeter) ones without
  symptoms are usually followed with repeated
  cerebral angiographies

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Treatment

• Ruptured aneurysms
• Surgical clip placed at the base of the aneurysm
• Aminocaproic acid may be considered, but has
  complications
• Calcium channel blockers such as Nimodipine may
  prevent spasm of the artery where the aneurysm
  ruptured

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STROKE
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Stroke

• 3rd Leading cause of death in the United States
• The mortality from the acute event is about 20
• Leading cause of disability

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Three Types of Stroke

• Temporary or partially occluded blood flow (TIA)
• Hemorrhagic stroke
• Ischemic (infarct) stroke

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Stroke - Type 1

• Temporary partial occlusion of blood flow
• TIA or Transient ischemic attack
• nonpermanent deficits
• 30 will have a stroke

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Management of TIA

• ASA
• Dipyridamole (Persantine)
• Ticlid
• Plavix
• Carotid Endarterectomy

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Stroke - Type 2

• Hemorrhage Stroke
• bleeding in skull or brain (subarachnoid or
  intracerebral)
• blood must be removed
• burst aneurysm
• (the worst headache of my life)

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Hemorrhagic Stroke

• Only 1 out of every 5 strokes
• 30-day mortality of 30-50
• Occur in younger patient population
• Two major categories -
• intracerebral
• subarachnoid hemorrhage

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ICH

• Majority of hemorrhagic strokes
• Leading risk factors - increasing age,hx of prior
  stroke
• Associated with
• Chronic HTN
• Amyloidosis
• Other causes -
• bleeding diathesis due to iatrogenic
  anticoagulation, vascular malformation and
  cocaine use

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SAH

• Half as common as ICH
• Half of all SAH due to berry aneurysm rupture
  most commonly occurring at arterial bifurcations
  or branchings
• Arteriovenous malformations make up another 6 of
  all SAH

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Stroke - Type 3

• Ischemic (infarct) stroke
• 70-80 of all strokes
• can be reversed with clot busters
• occlusion or blockage
• embolization (primarily from the carotid artery
  or the heart)
• thrombosis
• low flow state

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Ischemic Stroke

• Three Major Categories
• Thrombotic
• Embolic
• Hypoperfusion

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Ischemic Stroke
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Stroke

• Arteriosclerosis -
• what occurs in the heart can occur in the brain
  as well...

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CAROTID ATHEROSCLEROSIS

• The proximal internal carotid artery and the
  carotid bifurcation are most frequently involved
• Ulceration frequently occurs, placing the patient
  at higher risk for embolization or thrombosis

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Risk Factors

• Diabetes mellitus
• Obesity
• Family history

• Hypertension
• Hypercholesterolemia
• Smoking

• The risk of stroke from carotid disease is
  highest in patients who have recently sustained a
  reversible neurologic event, such as a transient
  ischemic attack

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Clinical syndromes

• Persistent, disabling neurologic deficit
• Non-disabling strokes
• Transient ischemic attacks (TIAs)
• Reversible ischemic neurologic deficits (RINDs)
• Less commonly, patients present with
  vertebrobasilar symptoms such as diplopia,
  dizziness, dysarthria, visual loss, dysphagia, or
  ataxia

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RIND

• Reversible Ischemic Neurological Deficit (RIND)
• Admit and observe for signs of neurologic changes
• Seizure precautions
• Repeat neuro exam and further studies I.e. repeat
  ct/MRI/ Doppler

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Evaluation of carotid artery stenosis

• Carotid duplex ultrasonography
• Transcranial Doppler
• Computed tomographic angiography
• Magnetic resonance angiography (MRA)
• Carotid angiography (the gold standard)

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ACUTE phase care

• Turn to affected side
• Elevate HOB with neutral head alignment
• O2
• Anticoagulants
• Possibly anticonvulsants

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ACUTE phase care

• prevent straining
• prevent agitation/restlessness
• BP management

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Diagnostics

• Look for risk factors
• Carotid Doppler
• Complete cardiac work-up
• LP
• CT Scan
• MRI
• EEG

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Differential Diagnosis of Acute Stroke

• Hypoglycemia
• Postictal paralysis (Todds paralysis)
• Bells palsy
• Hypertensive encephalopathy
• Epidural/Subdural hematoma
• Brain tumor/abscess
• Complicated migraine
• Encephalitis
• Diabetic ketoacidosis
• Hyperosmotic coma
• Meningoencephalitis

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What initial support should be given?

• Oxygen
• BP management
• Cardiac Evaluation

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What are the initial aids to dx and management ?

• Blood tests (blood sugar)
• ECG
• Pulse Ox
• non-contrast CT scan
• Lumbar puncture when CT normal and SAH suspect

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Other Tests/Studies

• MRI
• PET
• Doppler Study

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Early Management

• Ischemic Disease
• Consideration of thrombolysis
• Consideration of anticoagulation

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Early Management

• Primary intracerebral hemorrhage
• Consideration of operative intervention
• ventricular shunt
• Hematoma evacuation

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Early Management

• Subarachnoid hemorrhage
• Consideration of angiography
• Consideration of early operation

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T.P.A. - Thrombolytics for CVA

• When to Use
• Time to Drug From Onset of Symptoms
• Exclusion Criteria

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Tissue Plasminogen Activator (TPA)

• Medication approved by FDA for acute treatment of
  stroke
• Must be given within 3 hours of neurologic
  symptoms(numbness, tingling, weakness, speech
  problems, language difficulties), while awake

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Tissue Plasminogen Activator (TPA)

• IV r-TPA given in a dose of 0.9mg/kg up to a
  maximum of 90mg - 10 of the dose in a bolus and
  the remainder infused over one hour
• improves outcome after stroke when given very
  early and within 3 hours on onset of stroke in
  carefully selected persons.
• The benefit persists over the long term (3
  months)

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Tissue Plasminogen Activator (TPA)
Contraindications

• Patient selection and timing of symptoms are
  critical!
• Symptoms not rapidly improving or resolved
• No currently active internal bleeding
• No illness predisposing to an increased risk of
  bleed

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Tissue Plasminogen Activator (TPA)
Contraindications

• No history of prior brain hemorrhage
• No significant GI or GU bleeding in past 3 months
• No known stroke, serious head trauma, or brain
  surgery in past 3 months
• No lumbar puncture or arterial puncture in past
  week

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Tissue Plasminogen Activator (TPA) -
Contraindications

• No pregnancy
• Diastolic BP lt or 110 and systolic BP of lt or
  185
• Platelet count less than 100,000/mm3
• No Major surgery within preceding 14 days
• Blood glucose lt50mg/dl or gt 400mg/dl
• recent MI

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Unconsciousness

• A Alcohol or acidosis
• E Epilepsy/environment
• I Infection
• O Overdose
• U Uremia
• T Trauma
• I Insulin
• P Psychosis
• S Stroke/Seizures

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Seizures
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Seizures

• A short circuit of the brains electrical energy
• Effects vary depending what part of the brain is
  affected

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Seizures

• Epilepsy
• Head Injuries
• Hypoglycemia
• Hypoxia
• Poisoning
• Withdrawal

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Seizures

• Seizure Types (4 types)
• Grand mal
• Focal motor
• Petit mal
• Febrile

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Grand Mal

• Three phases
• Tonic - muscle rigidity
• Clonic-violent, rhythmic, jerking of extremities
• Postictal - decreased LOC

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Grand mal signs

• Loss of consciousness
• loss of bowel and bladder
• cyanosis or dusky appearance
• hypoxia from diaphragm seizing too

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Grand mal seizure emergencies

• Seizure lasts more than 5 minutes
• recovery from seizure is slow
• second seizure follows immediately (status
  epilepticus)
• person having seizure is pregnant
• Signs of illness or injury are present

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Focal Seizure

• Focal seizure (temporal lobe)
• 1-2 minute loss of consciousness
• bizarre behavior
• smacking of lips
• picking at things
• swallowing
• postictal like episode after

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Petit mal seizures

• Start with children 6-12
• Brief, sudden lapses in consciousness
• Small jerks of face or arms
• No post ictal period

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Febrile seizures

• High temperature
• 5 of children (6 months to 6 years)
• Can run in families
• Tylenol/Motrin

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What is the most appropriate work-up ?

• Most patients present with a motor convulsion -
  and are initially evaluated in the ED

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History

• Once it is determined that the patient had a
  seizure -
• In case of a previously documented evaluated
  seizure disorder - typical attack -little further
  evaluation is required
• Is patient taking anticonvulsant medications
• ? Any change in medication
• ? Missed dose,etc.

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History

• If there is no previous history of seizures a
  much more detailed hx is needed
• Any symptoms of previously unrecognized seizures?
  
• Any other neurologic symptoms?
• Any systemic illness ?
• Any drug ingestion/alcohol use?
• Family Hx?

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Neurologic Exam

• Evaluate patients level of consciousness and
  mentation - serial exams
• Any signs of increased intracranial pressure?
• Any focal weakness or reflex change?

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Neurologic Dysfunction

• Shortly after a seizure, this dysfunction can be
  identified which represents Todds paralysis
  (postictal focal cerebral dysfunction) and
  localizes seizure onset
• it resolves within minutes to hours

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Treatment

• ED treatment will vary depending upon the
  specific clinical situation
• Four scenarios
• The acute seizure
• Patient with previous epilepsy had a recent
  seizure
• Patient with first seizure
• Patient in status epilepticus

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Treatment

• Protect patient from harm (do not forcibly
  restrain)
• Roll patient on their side
• Do not put anything in their mouth
• they will not swallow their tongue
• bite it - maybe but not swallow it

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Treatment

• Protect patient from injury
• IV line established
• Endotracheal intubation -if necessary
• Nasogastric tube -if necessary
• Initial blood work-
• blood glucose, electrolytes, where indicated -
  serum toxicology screens and anticonvulsant
  levels
• In cases of prolonged seizure - CK levels and
  urine myoglobin should be done

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Treatment

• Lumbar puncture -rarely indicated (difficult)
• If bacterial meningitis suspect - empiric
  antibiotic therapy should be started
• Radiographic studies
• CT scan (delayed until seizure controlled)
• Thiamine /glucose given IV is hypoglycemia
  suspected/confirmed