Headache Flashcards
A 65 yo F presents to the ED with a complaint of headache. The patient is brought in by her husband. The patient states the headache is a 10/10 and started while she was carrying laundry up the stairs. The patient has a history of migraines, but this headache is ‘much worse and feels different’. She has vomited twice since the start of the headache and continues to be nauseated. She also has light and noise sensitivity. The patient also feels lightheaded and like she might ‘pass out’.
Most like subarachnoid hemorrhage
You suspect your pt has a subarachnoid hemorrhage, what labs do you order?
●Complete blood count
●Basic metabolic panel
●Coagulation studies
●EKG
●CT scan of brain (non-contrast)
Define Subarachnoid hemorrhage. What are they two types?
acute extravasation of blood into the space between the arachnoid membrane and the pia mater.
– Spontaneous SAH: rupture of focally weakened artery in the
subarachnoid space: Aneurysm
– Secondary SAH:
• Trauma: Hemorrhage may derive from several sources: trauma, Rupture or dissection of vertebral arteries, Intracerebral hematoma
Saccular (berry) aneurysm
– Not present at birth, but defect in____ is congenital and the aneurysm develops over time
– Increasing risk of rupture as _____
– Occur typically at branch points, 90% in the _____
media
size increases
anterior circulation
What are some increased risks for rupture or devo of Berry Aneurysms
Increased risk with hypertension, smoking, arteriovenous malformations, polycystic kidney disease, defects in vascular collagen, smooth muscle or elastic tissue (Ehlers- Danlos syndrome)
Aneurysm due to infection (bacteria or fungus)
Fusiform, atherosclerotic aneurysm: usually ______ arteries
Mycotic aneurysm:
vertebral basilar
Regarding pharmacologic management of your patient with subarachnoid hemorrhage, what are your goals for managing this patient’s blood pressure?
Avoid reducing blood pressure too much or too quickly
●Goal of SBP<150 or DBP <90mmHg or within 5% of baseline
Medications to initially manage subarachnoid hemorrhage
–Labetalol (beta blocker)
–Hydralazine (direct vasodilator)
–Nicardipine (Ca channel blocker)
–Esmolol (beta blocker)
Best way to deliver meds to pt with subarachnoid hemorrhage
i.v. to allow for titration of blood pressure
Why don’t we want to use nitrate or RAAS for pts with subarachnoid hemorrhage?
What do we need to keep in mind when giving Beta blockers?
- Avoid use of nitrates – increases ICP
- RAAS Inhibitors – too slow in onset
- β-Blockers – i.v. with short half-life that can be titrated and do not increase ICP
Role of B-1 receptors
– heart, kidney
– stimulation increases HR, contractility, renin release
Role f B-2 receptors
– lungs, liver, pancreas, arteriolar smooth muscle
– stimulation causes bronchodilation & vasodilation
– mediate insulin secretion & glycogenolysis
What B blockers are specific for B-1 receptor
Metoprolol and Atenolol
What B blockers cover B1 and B2 receptors
Propranolol and Labetalol
Understand B blocker mechanism in regards to regulating Blood Pressure
Start by blocking renin and decreasing HR
During a subarachnoid hemorrhage neighboring vessels may experience cerebral vasospasm, what can we use to tx this? how does it work?
CCB: use a Dihydropyridine, specifically Nimodipine
Nimodipine has selectivity for cerebral vascular smooth muscle cell Ca2+ channels
nifedipine, amlodipine, nimodipine are what kind of drugs
Dihydropyridine CCBs
Non-dihydropyridine CCBs
Diltiazem and Verapamil
You suspect your pt had a subarachnoid hemorrhage but the CT scan was negative, what would your next test be and why? Describe the findings on this test that would confirm a subarachnoid hemorrhage.
Lumbar puncture: we would expect to see xanthochromia
A 5 yo M presents via EMS after falling from a tree house in his neighbor’s backyard. The child is awake at this time, but was reported to be unresponsive immediately after the fall. He is in full c-spine and backboard precautions. He is crying and is trying to get up off of the backboard. He is noticed to have a laceration and hematoma to the right side of his head, bleeding is controlled. His parents are with him and are having a hard time consoling him. The patient has vomited twice en route to the hospital.
Dx?
Trauma: likely an epidural hematoma
Range of normals for pediatric vital signs
Note patterns, do not memorize
What is key for initial management of pt you suspect has an epidural hematoma
Airway, Breathing, Circulation, Disability, Examine, Fahrenheit, Get vials, Head-to-toe assessment, Intervention
Epidural hematomas are most often in the temporal region because:
– Bone is relatively thin in this area & more susceptible to fracture – Middle meningeal artery courses in this region & so is torn
Mechanism of epidural hematoma
Mechanism: dura is firmly adherent to inner table of skull
• May take time (minutes to hours) for the dura to come free from the
skull as hematoma grows (explains lucid interval)
What is the Cushing Reflex (triad)
– Increased Blood Pressure
• Sympathetic nervous system - vasoconstriction
– Decreased Heart Rate
• Parasympathetic nervous system – reflex bradycardia
– Irregular Breathing
• Compression of brain stem
How do you treat and manage increased intracranial pressure?
• Osmotic agents – mannitol does not cross blood brain barrier
– Dramatic decrease ICP 50% within 30 minutes
• Loop Diuretics – furosemide – Decrease ICP
Mannitol:
- _____ filtered
- Not reabsorbed
- Metabolically____
Freely
inert
What is the mechanism of mannitol?
Given intravenously only
Act in tubular lumen as non-reabsorbable solute
Urine volume and sodium excretion are proportional to the osmotic load
Increases the urinary excretion of sodium, potassium, chloride, water and mannitol
Uses of mannitol
Edema
Glaucoma-reduces intraocular pressure
Acute renal failure
Loops:
Orally and intravenously active
High efficacy (____of filtered sodium load excreted)
____in onset
____ duration of action
20-30%
rapid onset
short duration of action
MOA of Loop diuretics
Filtered and secreted by the OAT
Inhibits Na-K-2Cl symporter
Acts on the cortical and medullarymsegments of the ascending limb of the loop of Henle
Increase the excretion of sodium, potassium, chloride and water
What are my three loop diuretics
furosemide, Bumetanide, Ethacrynic acid
Subfalcine herniation:
what’s herniating and what structures are at risk of damage?
Cingulate gyrus herniates under the falx
Caused by asymmetric expanding hemispheric lesions
May cause in compression of ant. cerebral art. resulting in infarction
Medial temporal lobe displaced through the tentorial opening because of asymmetric expanding lesion
Uncal hernaition
4 complications of Uncal herniation
Ipsilateral 3rd nerve compression + pupillary dialation
Compression of brainstem (midbrain peduncle containing corticospinal tracts) against the tentorial edge opposite the direction of herniation (can lead to false localization of motor deficit- ipsilateral hemiparesis) (Kernohan’s notch)
Posterior cerebral artery compression (ipsi- or bilateral)
Duret hemorrhage
Why do you experience ipsilateral 3rd nerve compresion in uncal hernation?
the tentorium is firmly attached to the skull and taut. When the midbrain is pushed down from above it is pushed against the tentorium compressing the 3rd nerve.
Why is there pupillary dialtion in uncal herniation?
Pupillary constrictor fibers are located on surface of 3rd nerve
What is Kernohans notch (seen in uncal hernation)
With compression of the midbrain due to herniation from above the opposite cerebral penduncle is pushed against the opposite free edge of the tentorium
Causes weakness and a Babinski sign ipsilateral to the cerebral hemispheric lesion (because of crossing of corticospinal tracts in distal medulla)
Fatal brainstem hemorrhage
Secondary to progression of uncal herniation and resultant tearing of vessels in midbrain/pons
Duret hemorrhage
– Symmetric expansion of supratentorial contents into posterior fossa or
– Expanding mass lesion in posterior fossa
Cerebellar tonsillar herniation
Caudal cerebellar structures (“tonsils”) attempt to escape through the foramen magnum
Consequence of cerebellar tonsilar herniation
Medullary compression results in cardiorespiratory arrest
An 19 yo F presents to the ER with complaint of fever and headache. Her family is with her. She is home on Spring Break vacation from college, but the family feels that she is not acting like herself. She was feeling sick since she got home yesterday with headache, fever, chills, nausea and vomiting. Her mom has given her Tylenol for pain and her fever with only mild improvement in her symptoms. The patient is fully clothed in winter attire, but is shaking and complaining of feeling ‘cold’.
Lives with her roommate in a dorm at UW Madison ; Vitals: BP 95/60, HR 120, RR 24, Temp 102.4, Pulse Ox 99% room air , has Neck (Brudzinki and Kernig)
looks like meningitis
What is the Brudzinski sign?
the Kernig sign?
Brudzinski: when you flex pts neck, they bring knees to chest
Kernigs: can’t extend pts leg at the knee when thigh is flexed dt stiffness of the hamstrings
Cause of hyperacte meningitis
– Sparse inflammation, numerous organisms, congestion
– Meningococcalmeningitis
Cause of Acute (2-7 days) menintigits - most common infection in CNS
often bacterial with hematogenous spread
Cause of Subacute/chronic (> 1 week) meningitis
– Tuberculosis, syphilis (often brain parenchyma also affected)
– Lymphocytes, plasma cells, macrophages appear in exudate
Cause of “Aseptic” meningits
(usually viral) - much less fulminant than bacterial meningitis & less severe symptoms
– Summer&early fall
– Lymphocytic infiltrate in meninges
Characteristics of Neisseria
Gram negative diplococcus, aerobic
– Capsular polysaccharide biochemical structure determinesserogroup
• Six (of 13) capsular subgroups: cause almost all invasive meningococcal disease
What are the virulence factors in Neisseria
capsule and endotoxin structures
Trasnsmission of Neisseria
– 1-5% of exposed persons develop disease
– Transmission: direct contact with respiratory secretions or inhalation of respiratory droplets
- Crowding/closecontactincreasetransmission
- Disease occurs within 1 to 14 days of exposure and transmission
What is the progression for Neisseria Meningitis
– Meningitis: 40-65%
– Meningococcemia with shock (20-30%)
• Progression from initial symptoms to death may be hours
What is Meningococcemia
– Shock is dominant clinical picture
– Acute sudden-onset fever, malaise, weakness, cold extremities, pallor, leukocytosis or leukopenia, rash, headache, drowsiness, hypotension
• Rash: 40-80% cases
What causes the rash seen with Neisseria Meningitidits
bacteria in capillaries invade through walls and incite inflammation and bleeding resulting in petechiae that may progress to ecchymoses and eventually ischemic necrosis
What is Waterhouse-Friderichsen syndrome
massive bilateral hemorrhage into adrenal glands
Dx for Meningitis
isolation of bacteria or of antigen/DNA in blood, CSF or other body fluid
Disease seen in Neisseria Meningitidis
– Sudden-onset headache, fever, vomiting, myalgias, photophobia, irritability, agitation, drowsiness, meningeal signs (neck stiffness, Kernig’s or Brudzinski’s sign)
– With or without rash
– High concentration of organisms & inflammatory mediators in CSF.
What do we see in the subarachnoid space in bacterial meningitidis
Exudate present, numerous polymorphonuclear leukocytes, in subarachnoid space
Most common cause of Bacterial meningitidis in <3 months old
What do you tx with?
Strep agalactia, E. Coli, Listeria, S.Aureus
Ampicillin + Ceftriaxone OR cefotaxime
Most common cause of Meningiditis 3mo-18 yrs
what do you tx it with?
Neisseria, S. PNeumonaie, S. Aureus, H.flu
Cefotaxime OR ceftriaxone PLUS Vancomyocin
Most common cause of meningitis 18 yrs- 50 yrs
tx?
S. Pneumo, Neisseria, S. Aureus
Tx:
Ceftriaxone or Cefotaxime PLUS Vancomyocin
Tx for meningitis over age 50
S. pneunomiae, Listeria, S. aureus, Gram negatives
Ceftriaxtone PLUS Ampicillin PLUC Vancomyocin
Key points on transimission and prophylaxsis of Neisseria meningitidis
N. Meningiditis transmitted by exchange of respiratory and throat secretions (kissing, living in close quarters, exposed to patient secretions)
●Those caring for patients with suspected meningitis should wear mask with shield and gloves
●Exposed family/friends, health care workers at high risk should receive antibiotic prophylaxis
Prophylaxsis recommendations in those exposed to N.Men
see table
