Head Injury And ACS,Stroke And Headache

Question 1

State ten causes of secondary brain injury

Answer 1

Systemic Insults
Hypoxia (PaO2 < 60 mmHg)
Mortality of TBI pts with hypoxia = doubled
40% of TBI ED patients exhibit hypoxia during course
Hypotension (SBP < 90 mmHg)
Present in 33-35% of TBI patients
Results from hemorrhagic shock, cardiac contusion, tension pneumothorax, etc
Hypotension → ↓Cerebral Perfusion→↑Cerebral Ischemia →↑Doubles Mortality
Anemia 2/2 Blood Loss (↓Oxygen Carrying Capacity)
Hypo/Hypercapnia
Hyperventilation → ↓pCO2 Levels → ↑Serum pH → Cerebral Vasoconstriction → ↓Cerebral Blood Flow
Previously was a mainstay of treatment and will help to buffer an expanding hematoma in short-term, but will ultimately decrease cerebral perfusion to penumbra region and increase tissue death

Other Systemic Insults
Seizures
Electrolyte Abnormalities
Coagulopathy
Infection
Hyperthermia
Iatrogenic (Under-resuscitation)
Intracranial Insults
Intracranial Hypertension
Extra-axial Lesions
Cerebral Edema (Peaks at 24-48 hrs post injury)

Question 2

What is the Monroe-Kelli Doctrine with regards to normal cerebral regulation
How much of the cranial vault does the brain occupy?
How much of the body’s oxygen supply does the brain take?
How much of the cardiac output of the body does the brain take ?
What does the cranial vault contain
What is the formula for cerebral perfusion pressure or cerebral blood flow

Answer 2

Brain is a semisolid organ that occupies 80% if cranial vault
20% of the body’s oxygen supply
15% of cardiac output
Cranial Vault = Fixed in size by outer rigid skull
Contains brain tissue, blood vessels and CSF

Monroe-Kelli Doctrine
Defines the relationship between the volumes of the three compartments
The expansion of one compartment MUST be accompanied by a compensatory reduction in the volumes of the other compartments to maintain a stable intracranial pressure (ICP)

CPP = CBF = MAP – ICP

Question 3

What is ACS? What’s the difference between myocardial ischemia and infarction
What conditions characterize ACS?

Answer 3

Acute coronary syndromes (ACS). Are conditions characterized by the sudden onset of coronary insufficiency as a result of thrombotic occlusion of one or more coronary arteries.

Three such conditions are identified:

ST-segment elevation myocardial infarction
(STEMI).
Non-ST-segment elevation myocardial infarction (non-STEMI).
Unstable angina (UA).

Myo ischemia is reduced blood flow to heart due to an occlusion while myo infarction is complete cut off of blood supply to the heart due to an occlusion

Question 4

State ten risk factors for development of coronary artery disease

Answer 4

Hypertension
Diabetes
Dyslipidemia
Smoking
Positive family history of early MI
Advanced age
Male sex
Obesity
Metabolic syndrome
Sedentary lifestyle
High-fat diet

Question 5

What is the most classical symptom of ACs
State four other associated symptoms

Answer 5

The classic presentation of symptomatic ACS is that of left-sided or retrosternal chest pain.
Pain may radiate to the jaw, neck, back or down either upper extremity.

Associated symptoms:
Nausea
Vomiting
Diaphoresis
Dyspnea
Syncope
Palpitations

Question 6

Which group of people usually experience absent chest pain

Answer 6

In diabetic and elderly patients, chest pain itself may be absent. In some of these cases an “anginal equivalent” such as shortness-of -breath, lightheadedness or nausea may be present

Question 7

How is ACs diagnosed ?
What are you interested in the history of a person with ACS

Answer 7

History
Physical Examination
Electrocardiogram (ECG)
Serum Cardiac Markers

History:
Onset of pain (eg, abrupt )
Provocation/Palliation (which activities provoke pain; which alleviate pain)
Quality of pain (eg, sharp, squeezing)
Radiation (eg, shoulder, jaw, back)
Site of pain (eg, substernal, chest wall, diffuse, localized)
Timing (episodic, duration of episodes, when pain began)

Question 8

In an ST elevated MI, what’s the ECG configuration

Answer 8

History and Physical Examination
ECG: Ischemic ST elevation typically has a convex configuration, is limited to selected ECG leads.
Serum Cardiac Markers

Question 9

What are the types of primary brain injury and secondary brain injury

Answer 9

Primary Brain Injury:
Types of Primary Brain Tissue Injury
Cellular Injury Mechanisms

Secondary Brain Injury:
Systemic Insults
Intracranial Insults

Mechanisms of Traumatic Brain Injury
Skull Fractures
Extra-axial Fluid Collections
Intraparenchymal Hemorrhage
Subarachnoid Hemorrhage

Question 10

Secondary brain injuries are categorized into what two things?
What is the goal of the emergency department concerning the secondary brain injuries?

Answer 10

Secondary Brain Injury
Systemic or Intracranial processes that contributes to the primary brain injury cycle and results in greater tissue injury

Categorized into:
Systemic Insults
Intracranial Insults

Emergency Department:
Treatment Focused on limiting the extent of secondary brain injury

Question 11

the types of extra axial fluid collection in traumatic brain injury are epidural and subdural haematoma.
What type of vessels are involved in epidural and subdural hematoma ?

Answer 11

Epidural Hematoma:
Middle Meningeal Artery (36%)
Head Injury w/ LOC + Lucid Interval followed by deterioration
Classic presentation = 47% of cases
Lenticular Shape on CT

Subdural Hematoma:
Injury to Bridging Veins
Blood accumulation between dura mater and pia arachinoid mater
Increased risk in elderly and alcoholics due to decreased brain volume
Hyperdense crescent shaped lesion

Question 12

Subarachnoid hemorrhage is common in what type of brain injury?

Which type of hematoma has the presentation of a thunder clap headache or the worst headache they have ever experienced?
What investigation can you do for this type of hematoma?
What is xanthochromia

Answer 12

Subarachnoid Hemorrhage:
Disruption of subarachnoid vessels
Common in moderate to severe brain injury
Worse prognosis
Twice as likely as other head injured patients to suffer from death, persistent vegetative state or severe disability

Subarachnoid hematoma
Lumbar puncture,CT scan

For the Lumbar puncture :
U collect some of the CSF and spin it. Yellowish pigmentation will settle down after the spin
This Yellowish discoloration is called xanthochromia
This is a bedside test done to detect subarachnoid bleed

Question 13

What are the hallmark symptoms of traumatic brain injury
What are the three cardinal features of confusion?
State and define the types of amnesia? And what is amnesia characterized by?
What causes loss of consciousness?

Answer 13

Hallmark Symptoms:
Confusion and amnesia w/ or w/o LOC

Severe brain injury often characterized by decreased mental status and presence of neurological deficits
Patients may also deteriorate from mild to severe head injury during course of evaluation

Confusion:
Characterized by three cardinal features-
Disturbance of vigilance and heightened distractibility
Inability to maintain a coherent train of thought
Inability to carry out a sequence of goal directed movements

Amnesia
May be anterograde or retrograde - you forget what happened before the injury
Anterograde- you forget what happened after the injury
Often characterized by repetitive questioning, inability to follow commands, inability to retain information during medical evaluation
Amnesia will decrease slowly over time and small amount of memory deficit remains
No loss of biographical data
i.e. Name, etc. – typically the result of hysterical rxn or malingering
Duration does correlate with severity and outcome of head injury

Loss of Consciousness:
Results from rotational forces at the junction of the upper midbrain and thalamus that results in disruption of reticular neuron function and inability to maintain alertness
Presence of LOC is not a predictor of long term neuropsychiatric sequelae of head injury

Question 14

Who developed the GCS?
Within what timeline are you suposed to measure GCS after injury ?
Why should it be performed after adequate resuscitation?
What GCS classification is classified as mild head injury?
Which is moderate?
Which is severe?

Answer 14

Glasgow Coma Scale
Developed by Teasdale and Jennett in 1974
Originally designed for measure 6 hours after injury to provide long term prognostic information about mortality and disability
Now, standardized to measure 30 min after injury and repetitive measurements throughout patient’s stay
Should be performed after adequate resuscitation b/c scale is sensitive to hypotension, hypoxia, intoxication and pharmacologic interventions
Current Classification
GCS = 14-15 = Mild Head Injury
GCS = 9 – 13 = Moderate Head Injury
GCS < 9 = Severe Head Injury
Best prognostic indicator of outcome = CT Scan

If a patient has GCS 14 and then has a seizure, it’s no more mild head injury, it moves to a severe head injury

Usually, someone with GCS of 14 has confusion that’s why it’s not 15

Question 15

What is the full score for eye opening?
What is the full score for verbal? For motor?

Mention them all

Answer 15

Glasgow Coma Scale (GCS)
Eye Opening(4)
Opens spontaneously 4
Responds to verbal command 3
Responds to pain 2
No eye opening 1

Verbal(5)
Oriented 5
Confused: talks in sentences but disorientated 4 (so you ask Sir how are you? Or ask about time person and place and he says something entirely different about how his wife has left him and all. He’s confused but he’s speaking in sentences)
Verbalises: words, not sentences 3 (over here patient is confused but speaking in words. So sir how are you? No. His reply is just no. Or come or just a word. Patient is still confused but isn’t speaking in sentences but in words)
Vocalises: sounds (groans or grunts), not words. 2
No verbal response 1

Motor(6)
Obeys commands 6
Localizes to pain 5
Withdraws to pain. 4
Flexion to pain (Decorticate posturing) 3 (brings arms towards chest like when people put hands together to pray sort of)
Extension to pain (Decerebrate posturing) 2
No motor response 1

Question 16

What do you look for on neurological exam in TBI

Answer 16

Neurologic Exam:

Pupillary Size + Reactivity-
Fixed Dilated Pupil = Ipsilateral Intracranial Hematoma resulting in uncal herniation
Bilateral Fixed + Dilated = Poor Brain Perfusion, bilateral uncal herniation or severe hypoxia
Indicative of very poor neurological outcome

Neurological Posturing:
Decorticate Posturing = Upper extremity flexion with lower extremity extension
Cortical Injury above the midbrain
Decerebrate Posturing = Arm extension and internal rotation with wrist flexion
Indicative of brainstem injury
Very Poor predictor of outcome

Full, Complete Neurological Exam
Examine for subtle neurological deficits
Look for specific injury patterns:
Battle’s sign, CXF Otorrhea, CSF Rhinorrhea, Hemotympanum, peri-orbital Ecchymosis is indicative of skull fracture and is concerning for underlying brain injury

Question 17

State tensymptoms of mild head injury
(Cognitive,somatic,affective symtpms)

Answer 17

Mild Head Injury
• Signs and symptoms (early/late)
Signs and Symptoms of Head Injury
Cognitive:
Confusion

Anterograde amnesia
Retrograde amnesia
Loss of consciousness

Disorientation
Feeling “zoned out”
Feeling “foggy”
Vacant stare
Delayed verbal/motor response
Inability to focus
Slurred or incoherent speech
Excessive Drowsiness

Somatic:
Headache
Fatigue
Disequilibrium
Dizziness
Nausea/vomiting
Visual disturbances
Photophobia
Phonophobia
Difficulty sleeping
Ringing of the ears

Affective:
Emotional Lability
Irritability
Sadness

Question 18

Who developed composite grading system for head injury?

Answer 18

Grading scale for mild head injury with GCS =between 14-15 and concussion syndrome
Developed by Colorado Medical Society and American Academy of Neurology

Question 19

Explain the talk and die syndrome and what is the most common cause of this syndrome

Answer 19

Moderate
GCS = 9-13
Clinical presentation varies widely
10% of patients
Specialized Subset = “Talk and Die Syndrome”
Initially, talkative and without significant signs of external injury
Within 48 hours of injury, rapidly deteriorate
Epidural Hematoma is cause in 78-80% of cases
Patients with “talk and die syndrome” who present with a GCS > 9 but who deteriorate have been shown to have a worse outcome than patients who present with severe TBI at outset
? Delayed Diagnosis

Question 20

What is the early aggressive treatment of severe head injury?
What is the Cushing’s triad?
What is it characterized by?

Answer 20

GCS < 9
10% of patients with TBI
Early aggressive treatment is required with airway control, resuscitation, admission to ICU setting
25% of this patient population will require neurosurgical intervention
Outcome is poor with mortality as high as 60%
Exam typically with abnormal exam, often evidence of external trauma, abnormal pupillary exam and neurological deficits
Cushing’s Triad = Acute entity seen in severely head injured patients with significant increased intracranial pressure and impending herniation
Results from ischemia to hypothalamus with poor perfusion to the brain, resulting in sympathetic stimulation of the heart to correct poor perfusion. The sympathetic stimulation results in hypertension, but carotid baroreceptors respond with parasympathetic stimulation resulting in bradycardia

Characterized by:(wo PRI)
pulse low (Bradycardia)
relative or Progressive Hypertension(pulse looks low but bp looks very high)
Irregular or impaired respiratory pattern

Question 21

State two Multiple Standardized tools for evaluation of head injured sports player?
State the evaluation for head injury done at the ER

Answer 21

Standardized Assessment of Concussion (SAC)
Sport Concussion Assessment Tool (SCAT)

E.D. Evaluation:
Neurological Exam
Imaging such as:
Skull Radiography
CT Scan (Gold Standard)
Magnetic Resonance Imaging (MRI)
Experimental Modalities for Neuroimaging
Functional MRI (fMRI)
PET Scanning
SPECT Scanning
Magnetic Source Imaging (MSI)

Question 22

State four things skull radiography can evaluate for

Answer 22

Skull Radiography
Prior to CT, Skull radiography used as triage tool
Can evaluate for:
Skull fractures
Pneumocephalus
Blood in sinus
Penetrating foreign body
Patients with abnormal findings are at increased risk of intracranial findings

However, still misses a large number of patients with normal skull films but extensive injury
Limited utility at very rural sites without access to CT imaging

Question 23

State two rules used to identify patients who need CT
Note that these rules are for patients with a mild brain injury to check if they need a Ct but for patients with moderate to severe brain injury using GCS, do CT without the rules.

Answer 23

New Orleans Criteria
Canadian Head CT Rule

Question 24

State the New Orleans criteria (PV HAD a Seizure so we have to do a CT)

Answer 24

New Orleans Criteria
CT imaging is required for patients with minor head injury with any one of the following findings.
The Criteria only apply to patients who have a GCS of 15.
1. Headache (H)
2.Age > 60 years (A)
3. Drug or Alcohol Intoxication (D)
4.Persistent anterograde amnesia (P)
5.Vomiting (V)
6. Visible trauma above the clavicle(V)
7.Seizure(S)

The mnemonic HEAD CT’S can be used to remember the seven criteria: headache, emesis, age over 60, drug or alcohol intoxication, convulsion, trauma visible above the clavicles, and short-term memory deficits.

Question 25

What is the Canadian CT head rule? (DAM SATHAG)
Which people does it apply to?
What constitutes dangerous mechanism of injury?

Answer 25

Canadian CT Head Rule
CT Imaging is only required for patients with minor head injury with any one of the following findings.
The criteria apply to patients with minor head injury who present with GCS of 13-15 after witnessed LOC, amnesia or confusion.

SATHAG(H means high risk)
High Risk for Neurosurgical Intervention:
1.GCS < 15 at two hours after injury
2.Suspected open or depressed skull fracture
3.Any sign of basilar skull fracture (Hemotympanum, Peri-orbital Eccymosis, Otorrhea or Rhinorrhea, Battle sign
4 Two or more episodes of vomiting
5.Age > 65 years

(DAM. M means medium risk)
Medium risk for Brain Injury: Detection by CT Imaging
1 .Amnesia before impact of 30 or more minutes
2. Dangerous mechanism (E.g. Pedestrican vs. Motor vehicle, Ejection from motor vehicle or fall from an elevation of 3 or more feet or 5 stairs or fall from a place twice your height)

Question 26

Which of the head CT rules has a higher specificity?
What’s the difference between specificity and sensitivity (Abeg read the book or check notes)

Answer 26

Head CT Clinical Rules-
New Orleans Criteria
Sensitivity and Specificity of detecting a clinically significant CT finding
Sensitivity = 100%
Specificity = 24.5 %
Estimated to decrease CT imaging by 23%

Canadian Head CT Rule
Sensitivity and Specificity for need for neurosurgical intervention and clinically significant finding on CT imaging
Sensitivity = 100%
Specificity = 68%
Proposed to reduce CT scanning by 46%
Both decision rules have subsequently been validated

Question 27

How is mild head injury managed in summary?
What is goal of management of mild head injury?
State four risk factors for intracranial hematoma
What is done for people with mild traumatic brain injury and low risk features for intracranial hematoma

Answer 27

Mild Head Injury:
Admission Criteria
Discharge Criteria
Discharge Instructions
Return to Play Guidelines

Symptomatic treatment and prevention of secondary injury
Appropriate management depends on assessment of risk of neurological decompensation and risk factors for intracranial hematoma

Risk factors for intracranial hematoma-
Coagulopathy, Drug/Alcohol Intoxication, Previous neurosurgical procedures, Pre-trauma epilepsy or older age (> 60 y/o)

Low risk features
All patients with mild traumatic brain injury should be observed for 24 hours after that injury (either inpatient or outpatient).

Question 28

How is moderate and severe head injury managed?

Answer 28

Moderate and Severe Head Injury
General Principles
Airway Management
Hemodynamic Assessment
Seizure Prophylaxis
Operative Management
Intracranial Monitoring

In summary:
Do ABcs
Give oxygen
Hydrate
Elevate head
Prevent Coagulopathy
Prevent infections
Give anti seizure prophylaxis if indicated

Question 29

What is the admission criteria and discharge criteria for mild head injury

Answer 29

Admission Criteria
Hospital Admission is required for all patients at higher risk for complications including:
GCS < 15
Abnormal CT Scan
Seizure Activity
Abnormal Bleeding Parameters (Anticoagulation or bleeding diathesis)
Unable to be observed at home

Discharge Criteria
Low risk patients can be discharged home with oral and written discharge instructions
Patients can be discharged if:
GCS = 15
Normal neurological exam
Normal Head CT
No predisposition for bleeding

Question 30

What are the discharge instructions to be given to someone with mild head injury
State six warning signs after discharge

Answer 30

Discharge Instructions
Appropriate follow-up instructions should be provided both verbally and written instructions.
No need to awaken patient q 2 hours
Patients who return to ED due to persistent symptoms should undergo careful repeat neurological evaluation but little data supports repeat CT Scanning

Warning signs after discharge:
Inability to awaken the patient
Decreased/Altered mental status
Severe or worsening headache
Somnolence or confusion
Restlessness, Unsteadiness leizure activity
Visual difficulties
Change in behavior
Vomiting, fever, neck stiffness Urinary or bowel incontinence
Weakness or numbness

Question 31

What is the mainstay of treatment in moderate and severe head injury
How is the airway managed?
Why is nasotracheal intubation contraindicated in moderate and severe head injury?

Answer 31

General Principles
All moderate and severe head injured patients should undergo CT imaging
Stabilization and prevention of secondary insults is mainstay of treatment

Airway Management:
Prevention of hypoxia and hypoventilation key to preventing secondary insults
Patients with GCS < 9, should have endotracheal airway placed
Rapid Sequence Intubation is preferred method of intubation
Nasotracheal Intubation contraindicated due to tendency for ICP to increase 2/2 cough/gag
Lidocaine for prevention of increased ICP has not been shown to have a benefit
Special attention should be paid to maintaining cervical spinal immobilization

Question 32

How is the hemodynamic status assessed in moderate to severe head injury
Which fluids are contraindicated

Answer 32

Hemodynamic Assessment
Hypotension (SBP < 90) should be aggressively treated as significant cause of worse outcome
Rarely, hypotension is due to head injury itself and other traumatic injuries should be investigated
Treatment of hypotension is directed at maintenance of cerebral perfusion
Hypotonic fluids are contraindicated
Typically isotonic fluids are used (NS)

Sedatives, Analgesia and Neuromuscular Blockade:
Agitation is common finding and may result from pain, delirium or difficulties with oxygenation and ventilation
Minimizing agitation should be goal to limit increases in ICP or inabilities to oxygenate and ventilate
Typically, short acting opiates and benzodiazepines are utilized to decrease agitation
Long term sedation should be accompanied by sedation holidays to evaluate neurological exam (Diprovan, Midazolam)
Barbiturates are not typically used in the emergency department but do have a limited role in long term management of patients with increased ICP who require sedation and have failed other medical and surgical treatments for increased ICP.
Neuromuscular blockade is indicated for airway control with RSI but long acting blocking agents should be avoided because they limit serial examinations

Question 33

What are post traumatic seizures ?
State six risk factors for post traumatic seizures.(or state six indications for seizure prophylaxis in brain injury)
What is the anti seizure medication of choice?
How is raised ICP treated?
What is craniotomy

Answer 33

Seizure Prophylaxis
Post-traumatic seizures = Seizures occurring in less than 7 days post-injury

Risk factors = GCS < 10, Cerebral Contusion, Depressed Skull Fracture, EDH, SDH,Intracerebral bleeding, Penetrating head injury or seizure activity within 24 hours of injury

Brain Injury Foundation recommends anti-epileptic medications be administered to high risk patients for first 7 days post-injury
Acute management of seizure activity is managed with benzodiazepines and other typical anti-epileptic agents
No proven benefit to administration of anti-epileptic meds after 7 days to decreasing post-traumatic epilepsy

Phenytoin is the anti seizure medication of choice

Elevate the head by 30 degrees then
You give mannitol for the first 24 hours then you switch to a hypertonic saline???(check)

Question 34

Operative Management
Indications
Penetrating injuries or blunt injuries with breach of the calvarium/skull
Presence of expanding intracranial hematoma
Epidural Hematoma
If volume > 30 cm3 or if comatose (GCS < 9)
Subdural Hematoma
If size > 10 mm on CT or if 5 mm shift regardless of GCS score
Decompression if GCS decreases by 2 points from time of injury to hospital arrival
ICP > 20 mmHG or if pt with fixed, dilated pupils
Malignant cerebral edema
Operative Management
Decompressive Craniotomy
Salvage operation used to manage increasing ICP
Removal of part of skull and underlying dura
Decreases ICP, improves cerebral perfusion, prevents ischemia
Serves to limit secondary insults
Literature divided on true benefit
True or false

Answer 34

True

Question 35

What is the most frequent cause of death after a severe brain injury
What are the signs of a patient with raise ICP
What is the recommended ICP?
What is the initial first line treatment of raised ICP?
What’s the subsequent first line treatment?

Answer 35

Most frequent cause of death and disability after severe head injury - raise ICP

Identified in any patient with clinical signs of impending herniation, Cushing triad or rising ICP as identified by intracranial monitoring techniques
Recommended ICP < 20 mmHg with CPP > 60 mmHg

Initial First line treatment of increased ICP
HOB – 30 degrees

Subsequent first line treatment measures
Short term hyperventilation
Osmotic diuretic administration (i.e. Mannitol, Hypertonic saline)

Second Line Treatments
High dose barbiturates
Severe hyperventilation
Mild/moderate hypothermia
Decompressive craniotomy

Question 36

Explain second impact syndrome as a sequelae of head injury

Answer 36

Second Impact Syndrome
Rare, Controversial entity
Athlete who has sustained a mild concussion who subsequently suffers a second head injury before the symptoms from the first have resolved
Patients subsequently develop rapid diffuse cerebral edema (within 2 min), increased ICP and eventual herniation, coma and death
The first head injury is postulated to cause a disruption of the normal cerebral vascular autoregulation that causes increased cerebral blood flow, making the brain vulnerable to the second impact, when the rapid malignant swelling occurs
Return to play guidelines have been developed to prevent this type of secondary injury

Question 37

Explain some sequelae of head injury

Answer 37

Post Concussive Syndrome:
Constellation of symptoms that develops within 4 weeks of the injury and may persist for months (90% at 1 month, 25% at 1 year)
Treatment is with analgesia, anti-depressents and anti-emetics

Post-traumatic Epilepsy:
Seizure activity > 7 days from traumatic injury
Head trauma is cause of long term epilepsy in 3% of patients with epilepsy
Incidence is highest in patients with compound skull fracture, intracranial hemorrhage or presence of early acute symptomatic seizure (presence of all 3 factors increases risk by 50-80%)
Cannot be prevented with prophylactic use of antiepileptics

Persistent Vegetative State:
Rare complication of severe head injury, first described in 1972 by Jennett and Plum
Disruption of cerebral cognitive function with sparing of brainstem function
No awareness of themselves or environment and cannot interact with others but will maintain normal sleep-wake cycle
Recovery is rare if symptoms persist for > 3 months, no recovery documented after 12 months of symptoms

Question 38

State six ALARM symptoms for PUD

Answer 38

Alarm symptoms include GI bleeding, weight loss, early satiety, dysphagia or odynophagia, family history of upper GI malignancy, iron deficiency anemia or new upper GI symptoms in patients older than 55.