The Infographic Guide To Medicine Neeral L Shah Full Chapter

The Infographic Guide to Medicine
Neeral L. Shah
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The Infographic Guide to
MEDICINE
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NEERAL SHAH
A good infographic is worth a thousand words
Preface
As a medical student I always struggled reading numerous pages of text to try and pick
out details of diseases and therapies. Trained as an engineer, I found images flowcharts
and algorithms easier to understand. More recently, as a medical educator, I took notice
that many of my students also favored visually based materials to help provide a basis
for their learning. They often seek out these resources to provide them with quick
snapshots and commit high yield details to memory. At the same time, I had
encountered infographics that were being used to explain complex topics for the
purpose of patient education. I was surprised to learn that while infographics were being
used to convey information to patients, this modality was not being used in medical
education.
With my specialty training in gastroenterology and transplant hepatology, I set out to

develop a set of infographics for this field. With the help of two other physicians (Joseph
Mort and Joanna Odenthal), who were medical students at the time, we developed an
initial set of 29 infographics that covered major topics in gastroenterology and
hepatology. We studied the literature in graphic design for optimal layouts, space to text
ratios, and white space use. Keeping these guidelines in mind, we created and edited
an initial set of infographics. The weeks after we released this initial set of infographics,
many learners asked about their origin, inquired about access, and provided valuable
feedback. Word of mouth spread quickly and learners beyond our institution and in
other parts of the world were downloading our infographics. We surveyed some of the
initial users and found that 93% of survey participants reported the infographics being
useful. The top three reasons learners identified that they would use infographics were
knowledge reinforcement prior to patient care (55%), exam preparation outside of
patient care (26%), and knowledge reinforcement after patient care (10%). It seemed a
graphical summary of high yield clinical pearls could be used for exams, but more
importantly, to help improve patient care. The graphical nature allowed quick review of a
topic, and provided cues to recall previously learned material.
From this initial concept, and a partnership with McGraw Hill, I decided to expand the
topic areas beyond gastroenterology and hepatology. We enlisted the help of content
experts from many different fields in medicine and many technologically savvy medical
students (many from my own institution, the University of Virginia). With everyone’s
help, we were able to create this first edition, “The Infographic Guide to Medicine” that
covers over 600 topics. Coordinating the work of more than 13 associate editors and
over 75 students was challenging, but it was also rewarding to bring multiple viewpoints
to the final design. Each card we know has been reviewed by at least 4-5 people
looking to optimize the design and distill difficult concepts.
I am proud to say, to my knowledge, this is the first book dedicated to infographics for
medical education. These clear and concise infographics provide a great overview as
an adjunct to a learner’s foundational learning, and helps to solidify concepts in their
busy schedules. The culmination of this book would not have been possible without the
innumerable hours dedicated by medical students and associate editors from around
the United States. I also could not have completed this without the endless support of
my wife. I hope you are able to use these infographics as you create your own culture
and community of learning to ultimately provide better care to your patients.
Neeral L. Shah, M.D.
Copyright
The Infographic Guide to Medicine
Copyright © 2021 by McGraw Hill. All rights reserved. Except as permitted under the
United States Copyright Act of 1976, no part of this publication may be reproduced or
distributed in any form or by any means, or stored in a data base or retrieval system,
without the prior written permission of the publisher.
Book ISBN 978-1-260-45398-0
Book MHID 1-260-45398-7
This book was set in Minion Pro by KnowledgeWorks Global Ltd.
The editors were Amanda Fielding, Julie Grishaw and Christina M. Thomas.
The production supervisor was Richard Ruzycka.
Project management was provided by Harleen Chopra, KnowledgeWorks Global Ltd.
The cover designer was W2 Design.

Acid and Alkali Ingestion
Most injuries
occur at a pH
under 3 or over
11
Clinical Presentation
Eschar Stridor Children:
Drooling Vocal hoarseness Vomiting
Odynophagia/dysphagia Chest pain Refusing oral intake
Respiratory distress may be caused by edema of the upper airway, aspiration

Conditioning ofsubstance
of the caustic Training intoTasks
the tracheobronchial tree, or inhalation of fumes
Absence of oral burns does NOT exclude esophageal injury
Diagnosis and Workup

Acid or Alkali? Early endoscopy(within 12-24 hours
Detailed history to determine substance pH, of ingestion) for severe ingestions or
concentration, volume, and patient intent persistent symptoms
Acids = superficial coagulation necrosis Ingestion of lye in pediatric patient
Alkaline = deeper liquefactive necrosis
Check for coingestants in suicidal patients
omplications
Early: perforations leading to hemodynamic
instability/mediastinitis/subcutaneous emphysema
Late: scarring of pylorus and esophageal strictures
Reproduced with permission from Knoop KJ,
Increased risk of squamous cell esophageal cancer Stack LB, Storrow AB, et al: The Atlas of Emergency
Medicine, 4th ed. New York, NY: McGraw Hill 2016.
Photo contributor: Philip E. Stack, MD.
Management
Establish large-bore IV access and resuscitate with crystalloids
Manage airway and monitor for hemodynamic instability
Cricothyrotomy due to oropharyngeal
Oral intubation with direct visualization OR
edema, tissue friability, and bleeding
Contraindicated:
Activated charcoal/induced emesis (if caustic agent is only known ingestant)
Blind nasotracheal intubation Dilution/neutralization therapy
Copyright © 2022 by McGraw Hill. 107
03_Emergency Medicine_p105-190.indd 107 01/09/21 4:52 PM

Acute Abdomen
New-Onset, Severe Abdominal Pain Tenderness Often Requiring Surgical Intervention
Inflammation Perforation
Appendicitis Cholecystitis Bowel Perforation PUD, Diverticulitis,
IBD
age >55
Periumbilical to RLQ Pain Ruptured AAA

RUQ Pain
Rebound Tenderness “Four Fs” Young Female with
Ruptured Ectopic
+ β-hCG
Obstruction Ischemic
Bowel Obstruction Volvulus Mesenteric Ischemia Elderly
Atrial Fibrillation
Strangulated Hernia Bulging
Vomiting, Constipated Abdominal Mass
Secondary to Adhesions, Intermittent Pelvic
Ovarian Torsion
Hernia, or Malignancy Extremes of Age Pain; Young Female
Intra-abdominal Nonsurgical Extra-abdominal

PID MIMICS
Myocardial Infarction
Pancreatitis
Pulmonary Embolism
Nephrolithiasis
Pneumonia
UTI/Pyelonephritis
Management
Stabilize Patient
Reproduced with permssion
from Papadakis MA, McPhee SJ,
Obtain Diagnostic Imaging
Rabow MW: Current Medical
Diagnosis & Treatment 2019. Consider Antibiotics to Cover
Intra-abdominal Pathogens
New York, NY:
McGraw Hill; 2019.
Cholecystitis, Screens for Appendicitis, Consult with Surgical Subspecialty as

Screens for Perforation Obstruction,
Free Fluid (Free Air), Ruptured AAA, Appropriate for Definitive Therapy
(Ectopic, SBO (Air and Ischemic Pain Management
Trauma) Fluid Levels) Bowel

#1 Acute
Cause of acute
liver failure in
the United
Acetaminophen
States
Toxicity
Clinical Presentation Workup
Serum acetaminophen
Most patients are...
level
asymptomatic
Liver function tests, coagulation
But some may present with... tests
The above labs may initially be
normal
anorexia,
nausea, vomiting,
right upper quadrant pain,
liver failure,
hepatic encephalopathy,
renal failure, Helpful adjuncts:
metabolic acidosis, complete metabolic panel, drug
death screen, electrocardiogram
Management
Consider activated charcoal if If acetaminophen level = Possibly toxic per

presentation <1 hour status post- Rumack–Matthew nomogram...
ingestion
If single, acute ingestion, use...

N-Acetylcysteine (NAC)
Rumack–Matthew Nomogram
Repletes antioxidant
Treatment
Line glutathione
Serum If chronic ingestion, consider...

Acetaminophen
Time Status Post
Level
Ingestion NAC if serum acetaminophen level
or liver function tests elevated
Nomogram cannot be used for Liver transplant may be needed

levels <4 hours status post ingestion for severe cases (ie, fulminant
liver failure)
Acetaminophen level >150 mcg/mL at Survivors of acetaminophen toxicity

4 hours status post ingestion = Possibly toxic rarely have sequelae

Acute Appendicitis
Obstruction and subsequent inflammation and bacterial overgrowth of the vermis
appendix
Etiology
Fecalith (most common)

Lymphoid tissue
Tumors
Helminthic infection
Generalized abdominal pain that

moves to RLQ (McBurney’s point)
Reproduced with permission from Brunicardi FC, Andersen DK,
May be associated with nausea, Billiar TR, et al: Schwartz's Principles of Surgery, 11th ed.
vomiting, fever, anorexia New York, NY: McGraw Hill; 2019.
McBurney’s Point Diagnosis
Clinical diagnosis: Imaging for

surgical planning
CT for most. US or MRI for pregnant
or pediatric patients
Labs are frequently nonspecific but
may aid in excluding other diagnosis
Treatment
Most patients require urgent

appendectomy to prevent perforation
Pre-op patients should be given
antibiotics: cefoxitin,
piperacillin/tazobactam, or ceftriaxone
and metronidazole

Acute Isoniazid Toxicity
Active and latent Clinical diagnosis based on

tuberculosis treatment history of tuberculosis
treatment and seizure
Decreases mycolic acid
synthesis
One of World Health Helpful adjuncts: fingerstick
Organization's essential glucose, complete metabolic
medicines panel, toxicology screen,
electrocardiogram
May also decrease
γ-aminobutyric acid
(GABA) synthesis
Clinical
Presentation
Management
Clinical Use
Workup
Altered mental status, Vitamin B6 (ie, pyridoxine)

seizure, metabolic acidosis, facilitates GABA synthesis
coma, death
Benzodiazepines may also be

given to potentiate GABA
activity
Recurrent, refractory Supportive (ie, airway

seizures are management by assisting
pathognomonic oxygenation, ventilation, etc.)

Alcohol
Intoxication
Ethanol (CH3CH2OH)
Epidemiology Metabolism
Significant global impact

Ethanol absorbed in the stomach within
30-40% of all medical or surgical
patients have an alcohol-related health 30-45 minutes
problem Oxidation through alcohol
Alcohol use disorder estimated to affect dehydrogenase to acetaldehyde
Reduction of NAD to NADH
3-5% of the population
Mechanism Elimination
Increased GABA activity and decreased Oxidation follows zero-order kinetics

NMDA activity Concentration of alcohol in tissues has
Dopamine release contributes to its negligible effects on the rate of
addictive potential oxidation
Euphoria and disinhibition at lower In healthy individuals, metabolized at a
doses rate of approximately 150 mg of alcohol
At higher doses, respiratory depression per kilo of body weight per hour or one
and coma can occur drink per hour

Alcohol
Withdrawal
A life-threatening condition
Mild Withdrawal Alcoholic Hallucinations

Visual hallucinations without
Initial tremor
delirium present after more
High blood pressure
prolonged abstinence
Tachycardia
Anxiety/agitation Withdrawal seizures also
possible
3-36 hours (after last drink) 12-48 hours
Delirium Tremens Management

Most severe form of withdrawal
Visual hallucinations First line: Benzodiazepines
Severe autonomic hyperactivity Consider thiamine and folate
with vital sign abnormalities replacement for nutritional
Seizures deficiencies
Can lead to death
2-7 days EtOH & benzos activate GABA receptors

Anaphylactic Shock
Causes
Hymenoptera (eg, bee) stings
Food (eg, nuts)
Drug (eg, penicillin)
Plasma proteins in transfusion (patients
with IgA deficiency)
Echinococcus granulosus cyst rupture
Cascade
IgE degranulates mast cells
Histamine and tryptase released
Sudden drop in SVR & PCWP
Compensatory increase in cardiac output
Distributive shock (warm and dry)
Chemokines and cytokines cause tissue
damage
Care
Airway management
IM epinephrine (1:1000)
Anti-H1 and anti-H2
Steroids
MIMIC
Scombroid poisoning

Antiarrhythmic Toxicity
and Overdose
Class Ia Class Ib Class Ic
Sodium Channel Blockers Sodium Channel Blockers Sodium Channel Blockers
Lidocaine Flecainide
Disopyramide, Procainamide, Clinical presentation: Clinical presentation:
Neuro: Circumoral numbness, Dysrhythmia, hypotension
Quinidine tongue paresthesia -> anxiety -> Labs: Hyponatremia
Clinical presentation: seizure -> coma
Dysrhythmia, hypotension, Cardio: Hypotension, EKG: Prolongation of PR,
anticholinergic effects, SLE-like bradycardia, dysrhythmia QRS, and QTc. Ventricular
reaction (procainamide, chronic), Heme: Methemoglobinemia tachyarrhythmia and
cinchonism (quinidine, chronic) bradycardia
EKG: Normal QRS and short
EKG: Wide QRS and prolonged QTc Treatment *:
QTc Mainly supportive care
Treatment *: Treatment *: Consider lipid emulsion
Lidocaine Seizure precautions therapy for refractory
Sodium bicarbonate for Lipid emulsion therapy toxicity
hypotension
Class II Class III Class IV

β-Blockers Potassium Channel Blockers Calcium Channel
Amiodarone Blockers
Clinical presentation: Clinical presentation:

Bradycardia, hypotension, AMS Acute toxicity: Hypotension, Clinical presentation:
Labs: HYPOglycemia ventricular dysrhythmia, Bradycardia, hypotension,
bradycardia AMS
EKG: QRS widening Chronic toxicity: Pulmonary Labs: HYPERglycemia
(propranolol), heart block fibrosis, thyroid dysfunction, EKG: Heart block
corneal, hepatic, and cutaneous
Treatment *: toxicity (blue-gray discoloration) Treatment *:
Calcium Calcium
Glucagon EKG: Prolonged QTc Glucagon
High-dose insulin High-dose insulin
Consider lipid emulsion therapy Treatment *: Consider lipid emulsion
for refractory toxicity Magnesium to treat torsades therapy for refractory toxicity
*Supportive care (required by all):

General presentation: Treatments:
Airway management
Antiarrhythmic toxicity may cause QRS widening: Sodium bicarbonate
Breathing assistance
hypotension, dysrhythmias, and AMS QTc prolongation: Magnesium
Circulation support

Anticholinergic Toxicity
Causes of Toxicity:
Medications (ie, antihistamines, atropine); Mushrooms; Plants

(ie, Jimsonweed)
Tachycardia "Red as a beet" "Dry as a bone"

- Earliest & most reliable - Cutaneous vasodilation to - Sweat glands are innervated by muscarinic
sign!!!! compensate for loss of sweat production receptors, and thus anticholinergics produce dry skin
"Hot as a hare" "Blind as a bat" "Mad as a hatter" "Full as a flask"

- Interference with normal - Dilation and ineffective - Delirium; hallucinations - Reduced detrusor muscle
heat dissipation (sweating) accommodation that contraction and inhibited sphincter
leading to hyperthermia manifests as blurry vision relaxation leads to urinary retention
Evaluation & Management

1 Understand the clinical features of overdose
Tachycardia
Flushing, anhidrosis, hyperthermia, blurry vision (mydriasis),

agitated delirium, and diminished bowel sounds
2 Perform basic screening tests Diagnosis is based on clinical findings
Fingerstick glucose—to rule out hypoglycemia

Acetaminophen and salicylate levels—to rule out common coingestions
ECG—to rule out conduction system poisoning
Pregnancy test of all women of childbearing age
3 Manage anticholinergic toxicity

Stabilization of airway, breathing, and circulation
IV access, supplemental O2, cardiac monitoring, and continuous pulse oximetry
Antidotal therapy with physostigmine in the case of both peripheral
and moderate central toxicity
Symptomatic treatment as needed including sodium bicarbonate
(prolonged QRS or arrhythmias), benzodiazepines (agitation and
seizures), and possibly activated charcoal

Anticoagulant Toxicity and
Overdose
Classes: Vitamin K antagonists (warfarins), direct thrombin inhibitors,

factor Xa inhibitors, and heparins
Hemoptysis Widespread bruising
Bloody stools Fatigue
Lightheadedness Intracranial hemorrhage
Gross hematuria

For warfarins: Increased PT For heparins: Increased activated PTT (aPTT) is
within 24-72 hours is diagnostic diagnostic
For Xa inhibitors and direct thrombin inhibitors:

Specific labs are not available
Warfarins are also found in rodenticides!
Increased PT or PTT is suggestive but nonspecific
Other useful labs:

BUN, creatinine, CBC, blood
type, and cross-match
Management
For warfarins, use PO/IV vitamin K Idarucizumab reverses dabigatran (direct thrombin inhibitor)
(delayed effect) or FFP (immediate effect)
Andexanet reverses factor Xa inhibitors
Protamine reverses heparins
Vitamin K not indicated!
Support for serious bleeding:

FFP, prothrombin complex concentrate, blood product
replacement, or activated factor VII as needed

Anticonvulsant Overdose
Mechanism of Action
Enhanced GABA Calcium Channel Sodium Channel NMDA SV2A
Transmission Inhibition Inhibition Inhibition Stimulation
Benzodiazepines Lamotrigine Lamotrigine Lamotrigine Levetiracetam

Barbiturates Topiramate Topiramate Topiramate
Tiagabine Carbamazepine Carbamazepine Carbamazepine
Vigabatrin Valproic acid Valproic acid
Ethosuximide Phenytoin
Gabapentin Oxcarbazepine
Cardiac
Confusion Ataxia Nystagmus Seizure Hypotension
Arrhythmias
Workup and Management

Obtain drug history Activated charcoal
Electrocardiogram
Benzodiazepines for seizures
Basic metabolic panel
Sodium bicarbonate for QRS
Serum anticonvulsant concentrations prolongation
Ammonia level for suspected L-carnitine or hemodialysis for

valproic acid toxicity valproic acid overdose

Antipsychotic Overdose
Lethargy Hypotension Agitated Neuroleptic
Extrapyramidal
and and delirium and malignant Presentation
symptoms depends on the
sedation tachycardia confusion syndrome
specific
antipsychotic
ingested as well
as the patient's
age, tolerance,
and co-
intoxicants.
QTc Prolongation and Torsades des Pointes

Fingerstick EKG to rule out Acetaminophen
Serum
glucose to rule conduction system and salicylate concentrations of
the ingested
out hypoglycemia abnormality levels antipsychotic can
be obtained, but
these tests are not
readily available
or useful in the
acute setting.
Evaluation mainly consists of excluding other more harmful agents as the

cause of the patient's presentation.
Management
Activated charcoal if Treatment is
no contraindications primarily supportive Antipsychotic
overdose
generally has a
good prognosis.
The mainstay of
treatment is
supportive care.

Barbiturate Overdose
Duration Cl– channel open GABA CNS Activity
Clinical Presentation Diagnosis
Lethargy Mild - - - - - - - - - - - - - - - - Moderate - - - - - - - - - - - - - - - - Severe Specific Findings:

Patient history of barbiturate
ingestion
Slurred speech Urine drug screen
Nonspecific Findings:
Nystagmus
Skin bullae
Altered electrolytes, glucose, BUN,
Ataxia creatinine, arterial blood gas

Abnormal pulse oximetry, chest
radiograph
Bradycardia
Management
Hypotension
Supportive:
Protect airway and assist
Hypothermia
ventilation
Increase blood pressure
Diminished pupillary
Treat hypothermia
reflex/pinpoint pupils
Decontamination &
Respiratory arrest Elimination:
Activated charcoal
(if mental status allows)
Coma
Hemodialysis in severe cases
WARNING: Brainstem reflexes Urine alkalinization
may be suppressed and patient
may appear neurologically dead (phenobarbital only!)

Bee and
Wasp Stings
Uncomplicated
Local Reactions
Clinical Presentation Management
1-5 cm area of painful Remove stinger from wound if
redness/swelling present
Cold compresses
Develops within minutes, resolves
Oral antihistamine and topical
within a few hours/days
corticosteroids for pruritus
Large
Local Reactions
Exaggerated redness and swelling at sting Cold compresses
site that ENLARGES over 1-2 days Oral prednisone for swelling
NSAIDs
Peaks at 48 hours, resolves in 5-10 days
Oral antihistamines and topical
corticosteroids for pruritus
IgE-mediated
Anaphylaxis
Acute, life-threateningIgE-mediated type I hypersensitivity reactionaffecting
2 or more organ systems, or sudden hypotension after allergen exposure
Tachycardia IM epinephrine 1:1000

Vasodilation hypotension, edema Vasoconstriction
Bronchodilation
Upper airway edema stridor, hoarseness
Bronchospasm wheezing Airway management
Volume resuscitation
Urticaria, pruritus, flushing Adjunctive therapy
(antihistamines, H2-blockers,
Abdominal pain, nausea, vomiting glucocorticoids)
IgE-mediated

Benzodiazepine
and Barbiturate
Withdrawal
Shorter half-life drugs = quicker onset of withdrawal symptoms
Mechanism of Action
Decreased GABA receptor activation
Unchecked excitatory neurotransmitter activity
Sleep disturbances Delirium
Depression Seizures
Cardiovascular
Tremors collapse
Management
Support airway, breathing, and circulation
Restore GABA tone with long-acting

benzodiazepine/barbiturate, followed by slow
dose taper

Examples:
Alprazolam
Benzodiazepine Diazepam
Lorazepam
Clonazepam
Toxicity and Overdose Clorazepate
Chlordiazepoxide
Clinical Presentation: Sedative-Hypnotic

Toxidrome
Ataxia
Slurred speech
Minor respiratory depression
AMS (usually depressed)
Normal vital signs
Severe toxicity: stuporous or comatose
Diagnosis Urine
May NOT be detected
Clinical diagnosis
in standard urine
“coma with normal screening tests
vital signs” Urine screening test
designed to identify
Rule out other oxazepam & derivatives
causes of Positive test indicates
poisoning recent exposure, but does
NOT confirm toxicity or overdose
Management
Ensure airway is protected: intubation may be required
Oxygen as needed
Flumazenil: rarely used as it can precipitate withdrawal
seizures if patient is benzodiazepine tolerant
Naloxone: if concomitant use of opioids
Avoid activated charcoal if mental status is
depressed as it increases risk of aspiration

Beta-Blocker
Examples: Atenolol, Carvedilol, Labetalol, Metoprolol, Nadolol, Propranolol
Bradycardia & hypotension
Heart block Cardiogenic shock
Altered mental status, seizure, hypoglycemia
Other chronic/adverse effects: bronchospasm, erectile dysfunction, depression
Diagnosis
β-Blocker toxicity and overdose is a clinical diagnosis.
Rule out other causes of poisoning
ECG = bradycardia, PR prolongation, heart block
Labs = fingerstick glucose, serum chemistry (Ca, BUN, Cr)
Reproduced with permission from Hammer GD, McPhee SJ: Pathophysiology of Disease:
An Introduction to Clinical Medicine, 8th ed. New York, NY: McGraw Hill; 2019.
Complete Heart Block
Management
ABCs
Atropine & IV fluids
If severe—IV glucagon, calcium salts, and
hyperinsulinemia euglycemia therapy. Consider
pressors and lipid emulsion therapy for refractory
hypotension/bradycardia. Cardiac pacing may be
trialed but may not be effective
Supportive treatment—Sodium bicarbonate and
magnesium, IV dextrose (D50W), benzodiazepines

Blunt Abdominopelvic Trauma
Common Injuries Symptoms

Spleen Hypotension
Liver Tachycardia
Hollow organs Tenderness
Kidneys Guarding
Urethra Rigidity
Pelvic fracture
Trauma Workup Treatment

Airway Observe with
Ex Lap if:
Breathing serial exams if:
Peritonitis Negative FAST
Free air under Stable
Circulation
diaphragm Low-risk
Hemorrhage/shock mechanism of injury
Disability (GCS)
Exposure
Pelvic Fracture
Pelvic binder | Early resuscitation
Stable FAST CT
Surgery if:
Unstable FAST OR Open/unstable
fracture
X-ray pelvis Urologic injury
X-ray spine Hemorrhage
Complications
High risk of thrombosis Abdominal compartment Post-op infection

Shock
for pelvic injuries syndrome

Blunt Chest Trauma
Injuries Signs & Symptoms
Rib fractures/flail chest Hypotension
Hemothorax Tachycardia
Pneumothorax Rapid deceleration Chest pain/SOB
Pulmonary contusions is the most
Blunt cardiac injury Dysrhythmia
common JVD
Aortic disruption
Splenic/liver laceration mechanism for Murmurs
Tracheobronchial injury blunt cardiac injury Breath sounds
Workup Treatment Stable

Normal ECG Cardiac monitoring with
& no major reassessment for 4-6 hours &
ECG CXR FAST Troponin injuries repeat ECGs
ultrasound
Consider ABG and lactate Discharge home if no Abnormal ECG, then admit
change with telemetry
CK-MB has no predictive value Unstable

Serial troponin, ACLS algorithms
Troponin elevation cardiac monitor Rib fractures analgesia & O2
for dysrhythmias Chest tube if PTX/HTX suspected
Aortic disruption permissive hypotension
Unstable, signs of severe Echo (sys <120) and permissive bradycardia
injury, or abnormal ECG CTA Intrabronchial bleed bronchoscopy
Inotropic support
Water-soluble Surgery if: tracheobronchial, aortic, valvular,
Concern for
contrast myocardial, diaphragmatic, papillary muscle,
esophageal injury
esophagogram chordae tendineae, or coronary vessel injuries
Complications
Formation of Shock & Acute HF, valvular dysfunction, Dressler's

aneurysms or fistulas dysrhythmias or cardiac free wall rupture syndrome

Blunt Head Trauma
Common Injuries Signs & Symptoms
Brain contusion Altered mentation
Bleeding (subdural, epidural, intraparenchymal,
Focal neurologic deficit
intraventricular, subarachnoid)
Hypertension
Diffuse axonal injury
Bradycardia
Edema
Irregular
Skull fracture
respirations
Consider C-spine injury → spinal precautions Headache
Workup Treatment
Neurologic exam
MAP goal >80
Intubation & sedation (etomidate or propofol) if

Determine pupillary response:
patient uncooperative or combative
Fixed, dilated → uncal herniation
Bilateral pinpoint → opiates, central Primary Goals
pontine lesion, cerebellotonsillar
Secondary Goals
herniation Maintain cerebral Prevent secondary injury by
perfusion correcting:
Optimize intravascular Hypoglycemia
CSF leak increases risk for
volume Hyperglycemia
meningitis → PPx antibiotics
Optimize ventilation Hypoxia (SpO2 >90%)
Prevent and control Hypercapnia
CT rules seizures Hyperthermia
1. New Orleans and Treat elevated ICP (HOB Hypoperfusion
Canadian head rules 30°, mannitol, hypertonic
2. NEXUS and Canadian saline, etc.)
C-spine rules
Neurosurgical consult for: intracranial mass
lesion, ICP monitoring, ventriculostomy
Complications
Irreversible Infection (eg, Amnesia, cognitive, and/or Chronic traumatic

neurologic deficits meningitis) behavioral changes encephalopathy

Others living in the same house
presenting with the same
symptoms at the same time
Smoke inhalation
or other appliances
100
Normal
80 Irreversible
% Hemoglobin (Hb) saturation

CO binding
to Hb reduces
Colorless, odorless gas

Hb available
60 to bind O2
Carbon monoxide competitively binds to hemoglobin with 40 CO poisoning
200× the affinity of O2 20 Left shift with

CO reduces
O2 unloading
Does not affect dissolved O2 (PaO2) 0 20 40

PO2 (mm Hg)
60 80 100
Reproduced with permission from Kibble JD, Halsey CR: Medical

Physiology: The Big Picture. New York, NY: McGraw Hill; 2009.
Nonspecific
Red skin is a very late
Headache sign and is rarely seen
Confusion Seizure in living patients
Nausea Coma
Dizziness Death
Diagnosis SpO2 will be falsely

Arterial blood gas with serum carboxyhemoglobin (COHb) level elevated
Normal COHb May also have COHb levels may not

<5% in nonsmokers Anion gap metabolic acidosis correlate with symptom
<10% in smokers Lactate severity or prognosis
Creatinine phosphokinase
Troponin
Ischemic EKG changes
Management Consider hyperbaric oxygen therapy for:

100% oxygen until COHb >25%
Pregnant patients with COHb >15%
symptoms resolve
Severe symptoms including syncope, altered
Supportive care
mental status, focal neurologic deficit,
myocardial ischemia, seizure, or coma

Cardiogenic
Shock
Causes
• Acute myocardial infarction

• Heart failure
• Valvular dysfunction
• Cardiomyopathy
• Myocarditis
• Arrhythmia
• Hypotension (SBP <90 mm Hg)
•Not always withchest pain
• Cold, clammy, tachypnea, JVD
• Heart rate
• Tachycardia (compensatory)
• Bradycardia (infarcted AV node)
Physiology
Preload CO Afterload
• Narrow pulse pressure

• Insufficient pumping ability to support the
oxygenation of the tissues
Diagnosis & Treatment

• EKG and ECHO
• Chest radiograph
• Labs: troponin, lactate, CMP, BNP
• Treatment targeted at cause:
- Inotropes: dobutamine, dopamine
- Diuresis: furosemide
- Mechanical: aortic balloon pump

Cocaine and Amphetamine
Toxicity
Among Most
Sympathomimetic Commonly Used
Toxidrome Illicit Substances
Worldwide
Mydriasis
Rhabdomyolysis,
Renal Failure
Anxiety, Agitation, Clinical
Hallucinations Manifestations
Seizure
Hypertension,
Tachycardia,
Tachypnea, Cerebrovascular
Hyperthermia Accident
Complications
Arrhythmia
Chest Pain
Acute Coronary
Urine Drug Screen Syndrome (ACS)
(eg, Myocardial
Infarction), Aortic
Workup
Dissection
EKG
Supportive (ie,
Oxygen, IV Fluids)
CBC, CMP,
Troponin,
Creatine Kinase
Management Benzodiazepines
Chest X-Ray, Chest

CT Angiogram (as Avoid β-Blockers
needed) to Prevent
Unopposed
α-Agonism
Chest Pain with Concepts

Cocaine Use
Warrants an ACS Cocaine-Related ACS
Workup Management Same
as Non–Cocaine
Related ACS
(ie, Aspirin,
Nitroglycerin,
Reperfusion)

Cocaine and Amphetamine
Withdrawal
Clinical Presentation:
Depression/anhedonia
Lethargy
Drug craving
Increased appetite
Sleep disturbances (insomnia or
increased sleep)
Vivid nightmares (increased REM)
Drug Screen Times:

Diagnosis Blood and urine screens may
help identify recent drug
Clinical diagnosis exposure, but cannot
diagnose withdrawal
“Postuse crash” without clinical picture
Urine drug screen Urine screen may be
Blood screen positive up to 4 days
Rule out other after exposure
Blood screen may be positive
causes of poisoning
up to 1 day after exposure
Management
Symptoms typically Consider Using:
begin within hours of Benzodiazepines
Antidepressants
drug cessation, peak in Antipsychotics
1-2 days, and decrease Naltrexone
by 2 weeks Behavioral
therapy
Supportive care
Consider referral to drug rehab

Cyanide
Toxicity
Exposure
Smoke inhalation from burning
synthetic products
Shortness of breath, agitation, and
Industrial products: metallurgy, tachycardia
photographic development
Progresses to seizures, coma,
Natural sources: cassava hypotension, and death
processing, bitter almonds,
peach pits Symptoms occur within minutes of
exposure
Mechanism Patient may smell like

of Action bitter almond odor (not reliable)
Patients are not cyanotic

appearing!
Diagnosis and
Workup
Inhibits oxygen utilization in electron
transport chain leading to lactic acidosis Severe metabolic LACTIC acidosis
and hypoxia
Normal O2 saturation; elevated venous pO2
Cyanide level not clinically useful

Management
Treatment: If cyanide toxicity is from a fire, test
Airway, Breathing, Circulation carboxyhemoglobin level for carbon
Hydroxocobalamin (preferred) monoxide poisoning
Amyl nitrite or sodium nitrite
followed by sodium thiosulfate Assume patients in house fires have
cyanide poisoning
Complications:
Parkinsonism symptoms

Digoxin Toxicity
Etiology
Failure to adjust dose

NARROW to renal function
Physiology & Mechanism

K+
Na+
Increases intracellular calcium Shortens repolarization
Na+-K+-ATPase pump Increases inotropy Lengthens SA/AV conduction
Clinical Presentation & Diagnosis
Acute: HYPERkalemia Blurred
Bidirectional VTach
Management

UTI or Indwelling
Pyelonephritis Catheter
Atelectasis
11% Pseudomonas
Pneumonia
Replace or
Remove Foley
Incentive Catheter
WIND WATER
Spirometry
Antibiotics for
Symptomatic
Patients
Chest Physiotherapy
Surgical Site
Infection (up to 90
days for prosthetics)
Comorbidities
(diabetes, obesity,
or Abscess
Fever
or weak immune After Drug
system)
Surgery Reaction
Age,
Malnutrition,
tio
on Serotonin
Smoking
moking Syndrome
WOUND WONDER
DRUGS
Neuroleptic
Contaminated
ontam or Malignant
Long
Lon Surgery Antibiotics Syndrome
(Streptococcus,
Ultrasound
Staphylococcus, Malignant
or CT
Enterococcus) Hyperthermia
od rs Fever Before
Consider Blo inne
Withdrawal T h POD3
(Delirium Tremens) Aseptic
Womb
(Endometritis) Clostridium or
DVT β-hemolytic
Wonky Glands WALKING History of
(Adrenal Cancer, Obesity Streptococcus
Insufficiency or (ICU)
Thyrotoxicosis) Big
Abdominal Trauma (spinal
or Pelvic cord injury)
Leg Bone
Surgery
Surgery

Fibrinolytic Overdose
Pharmacology and Indications
Tissue Plasminogen
Streptokinases
Activator Analogs (tPA)
Alteplase, Reteplase, Tenecteplase Natural Streptokinase, Anistreplase Urokinase
Used for clot-related conditions Alternative to tPA Used only for

such as ischemic stroke, acute Lower cost, but worse pulmonary
myocardial infarction, side effect profile embolism
pulmonary embolism
Antigenic
Intracranial Catheterization Gastrointestinal Wound Epistaxis

Hemorrhage Site Bleeding Bleeding Bleeding
Management
Fibrinogen
Packed Red
Concentrate Aminocaproic Tranexamic
Blood Cells
and/or Fresh Acid Acid
(as needed)
Frozen Plasma

Heavy Metal Toxicity
Mercury Arsenic
Exposure: Exposure:
Elemental: Thermometers, dental amalgam Contaminated soil, water, food, industrial
Inorganic: Chemistry sets/antiseptics applications (metal alloy plating), medicinal,
Organic: Seafood and suicide/homicide attempts
Presentation: Presentation:
Elemental (inhaled): Respiratory distress Acute: Rice water diarrhea, garlic odor, QT
Inorganic: GI symptoms, renal failure, tremor, prolongation. Cardiogenic shock. Multiorgan
neurasthenia, erethism failure
Organic: Delayed neurotoxicity Chronic: Cancers, hyperpigmentation
Diagnosis: Diagnosis:
Urine, blood, hair, fecal Urine, hair, nails
Treatment: Treatment:
Dimercaprol, succimer Dimercaprol, succimer
MOST

IMPORTANTLY
REMOVE
Copper Gold
EXPOSURE!
Exposure: Fungicide, algicide, Exposure:
industrial uses, chemistry sets Treatment for rheumatoid
arthritis. Electroplating
Presentation:
Presentation:
Acute: GIdistress and perforation. Blue
Acute: Mucocutaneous (dermatitis, pruritus,
vomit. Jaundice
urticaria, stomatitis); metallic taste,
Chronic: Common in children from copper-
enterocolitis; Renal: Glomerulonephritis;
contaminated water. Similar to Wilson’s
eosinophilia; GI: Hepatotoxicity, pancreatitis
disease. Childhood cirrhosis. "Vineyard
encephalopathy, interstitial pneumonitis
sprayer’s lung" leads to adenocarcinoma
Chronic: Dermal chrysiasis, ocular chrysiasis,
cytopenias
Diagnosis:
Primary: Clinical diagnosis
Diagnosis: Clinical diagnosis, tissue biopsy,
Secondary: Copper levels in blood, urine,
hair, nails
elevated serum ceruloplasmin
Treatment:
Treatment:
Consider D-penicillamine
D-penicillamine, dimercaprol

Hyperthermia
>40˚C
(>104˚F)
Narrow Diagnosis with Focused History & Physical
Environmental
Exertional Nonexertional
Rapid onset Prolonged exposure
Athletes Elderly
Military Infants
Infectious & Drug Induced

NMS (antipsychotics)
Overdoses
Serotonin syndrome
Malignant Inhaled anesthetics
Hyperthermia Succinylcholine
Neuroendocrine
Evaluate mental status Thyroid
Stroke DKA
Intracranial hemorrhage
Seizure
Treatment
Treat underlying etiology of hyperthermia
Antipyretics
Cooling blankets Benzodiazepines NMS/SS
Cold IV fluids Dantrolene MH
Submersion ice bath Thyroid storm β-Blocker,
Gold standard PTU

Hypomagnesemia
Less intake: malnutrition, small bowel dysfunction,
C TPN, PPIs, EtOH

More excretion (outpatient): loop/thiazide diuretics,
A vomiting/diarrhea, hypercalcemia, EtOH,
U
hyperaldosteronism, Gitelman, Bartter, familial
HHNC, aminoglycosides, tacrolimus, cyclosporine
S
More excretion (inpatient): NG suction,
amphotericin
E Serum shifts: DKA treatment, acute pancreatitis,

refeeding syndrome, postparathyroidectomy
Exam: tetany, Chvostek sign, Trousseau sign,
hyperactive reflexes, tremor, fasciculations,

S
weakness, hypertension (preeclampsia), seizures I
ECG: flat T waves, U waves, long QT
(hypokalemia), arrhythmia, torsades de pointes

G
Labs: hypokalemia, hypocalcemia, dysglycemia N
S
T IV (over 12-24 hours except in renal insufficiency)
cie cy
cie y)
R PO (magnesium gluconate)
E Replete potassium and calcium
A Consider potassium-sparing diuretic if hypervolemic
T
Discontinue PPI
M
Diet: green leafy vegetables, nuts, legumes, seeds,
eds
d
ds
E
N whole grains

Hyp thermia
Causes
Environmental exposure
Hypoglycemia
Hypothyroidism
Adrenal insufficiency
Sepsis
Trauma <35˚C (95˚F)
CORE Body Temperature
Signs & Symptoms
Shivering (stops below 32°C)
Frostbite (soak in warm water
J (Osborn) Waves
Classic ECG Finding
bath to thaw)
Confusion
Lethargy -> coma
Cardiac arrhythmias
Management
32-35°C: Passive external rewarming
with removal of wet clothing and
application of blankets Reproduced with permission from Knoop KJ, Stack LB, Storrow AB, et al: The Atlas of
Emergency Medicine, 5th ed. New York, NY: McGraw Hill 2021. Photo contributor:
Michael L. Juliano, MD.
28-32°C: Active external rewarming

with warm water immersion or forced
warm air heating blankets No patient is dead until
they are warm and dead.
<28°C: Active internal rewarming with Do not stop resuscitation
warm IV fluids and consideration of efforts until patient has
thoracic/peritoneal lavage or ECMO been warmed!

Iron Causes
Majority are unintentional
Salts
Prenatal vitamins and
ferrous sulfate tablets can often
be bright and attractive to children
Toxicity Containers left open or improperly

closed not in a child-safe location
Intentional ingestion
Range of Toxicity
<20 mg/kg 20-60 mg/kg >60 mg/kg

Asymptomatic May be
Potential for
symptomatic
serious toxicity
Death can occur
Mechanism of Toxicity Clinical Presentaon

Mucosal cell necrosis
Impairment of capillary permeability
Abdominal Pain
Alteration of lipid membrane of
mitochondria Vomiting
Inhibition of Krebs cycle
Uncoupling of oxidative Diarrhea
phosphorylation
Direct vasodilation
Inhibition of proteases (eg, thrombin)
GI Bleeding
Serious Toxicity Can Cause: Renal and Neurologic Dysfuncon

Metabolic Acidosis
Mulsystem Organ Failure
Liver Failure
Shock
Bowel Obstrucon (delayed)
Management GI decontamination if there are
Prevention multiple radiopaque pill fragments
Supportive care—ABCs IV deferoxamine for serious
ingestion(iron level >500 µg/dL)

Mammalian Bites
Common Bugs Workup
Staphylococcus and
Assess for proximity to
Streptococcus
underlying structures
Pasteurella multocida
Distal pulse, motor, and
Capnocytophaga canimorsus
sensation
Anaerobes
Often polymicrobial Exam or 2D imaging for foreign
bodies
Rabies most common with
raccoons, skunks, & bats XR indicated for all infected
puncture wounds
Wounds >6 hours old with increasing CT or MRI for persistent pain or
pain and redness are likely infected failure to respond to therapy
Special Cases
Herpetic whitlow Rodent bite
Osteomyelitis Septic arthritis
Rat-bite fever rare
3-10 day incubation period
Immediate surgical referral Reproduced with permission from Wolff K,
Johnson RA, Saavedra AP, et al: Fitzpatrick's Color
Rigors and fevers
Withhold antibiotics until operative
Atlas and Synopsis of Clinical Dermatology, 8th ed.
New York, NY: McGraw Hill; 2017.
Migratory polyarthralgia +
debridement cultures obtained Hand bite from petechial or purpuric rash
Antibiotics should cover human with HSV 10-15% mortality without IV
Staphylococcus and Pseudomonas Acyclovir × 7-10 PCN 5-7 days
days
Risk Factors for Puncture Treatment

Wound Complications
Meticulous wound care → ↓ infection rate
Elderly
Diabetes Antibiotics if high risk of complication:
Immunocompromised Amoxicillin-clavulanate
Peripheral vascular disease
Contamination (soil, debris) Tetanus prophylaxis
Hand or foot wounds
Deep or crushing dog bites High-risk rabies
Puncture wounds from cats PEP: Ig + vaccine
exposure
Human bites
Early infection
Observe healthy domestic animals for
Treatment delay >12 hours
10 days
Leave deep puncture wounds open

Methanol and Ethylene Glycol Toxicity
Pathophysiology Clinical
Toxic Metabolite: Inebriation, ataxia, coma
Cloudy, blurred vision,
Formate/Formic Acid snowstorm in visual
field
Toxic to the optic nerve Retinal edema
Headache, nausea,
vomiting, abdominal pain
Methanol
Diagnosis Treatment
Fomepizole—inhibits
Clinical suspicion
Ingestion of alcohol dehydrogenase
Ethanol—competes for
Elevated osmolar gap antifreeze, paint alcohol dehydrogenase
Severe anion gap solvent, windshield binding
metabolic acidosis Hemodialysis
washer fluid
Ethylene
Glycol
Toxic Metabolite: Inebriation, ataxia, coma

(CNS stage)
Glycolate/Glycolic Acid Tachycardia, tachypnea,
Oxalate/Oxalic Acid hypertension
Nephrotoxic (Cardiopulmonary stage)
Acute tubular necrosis Flank pain, CVA
Oxalate crystalluria & tenderness, renal failure
calcium oxalate stones (Renal stage)
Pathophysiology Clinical

Methemoglobin Toxicity
Physiology Etiology
1. Oxidation of heme Accelerated oxidation
group(s) Fe2+ → Fe3+, due to medications:
which cannot carry oxygen Benzocaine
Lidocaine
2. Remaining heme groups
Nitroglycerin
have higher affinity for Sulfamethoxazole
oxygen Nitrate-based preservatives
3. Oxygen–hemoglobin Dapsone
dissociation curve Genetic predisposition:
shifts Left (Low Cytochrome b5 reductase
oxygen release) deficiency
4. Tissue hypoxia G6PD deficiency
Similar to acute anemia:

Dizziness
Shortness of breath
Headache Intravenous Methylene Blue
Palpitations reduces Fe3+ → Fe2+
Seizures (*note: give Methylene blue for
Coma Methemoglobinemia)
Vascular collapse
Severe metabolic acidosis Exchange transfusion for
Elevated methemoglobin level resistant cases
Pulse oximetry is unreliable
Chocolate-brown arterial blood
Clinical Treatment
Presentation

Neurogenic Shock
Baroreceptors
Medulla
CN IX
High-Impact Trauma CN X
DVPs
Cervical
HR (PNS)
HR (SNS)
Level of
injury
SPNs
Thoracic
Arterioles
Spinal Anesthesia SPN
Lumbar
Spinal cord injury (typically T1-L3)

Loss of sympathetic tone
Decreased vascular resistance leading to hypotension Decreased

Bradycardia and bradycardia. Peripheral vascular pooling will lead Urinary Output
to warm extremities but systemic hypothermia
Secure Airway Fluid Resuscitate Hemodynamic Support

30 cc/kg
Vasopressors (NE, dopamine,
phenylephrine)
Atropine
Rule out other causes of
Reproduced with permission from Butterworth JF,
Mackey DC, Wasnick JD: Morgan & Mikhail's Clinical
shock
Anesthesiology, 6th ed. New York,
NY: McGraw Hill; 2018.

Niacin Deficiency
Dermatitis Dementia
Pellagra
Clinical
Presentation
The 4 Ds
Reproduced with permission from Kang S,
Amagai M, Bruckner AL, et al: Fitzpatrick’s
Dermatology, 9th ed. New York, NY: McGraw Hill; 2019. Death
Diarrhea
Other
Glossitis
Disorientation
Insomnia
Risk Factors Diagnosis
A Alcoholism Serum niacin, tryptophan,

NAD/NADP ratio
B Bariatric surgery
Urine
N-methylnicotinamide
C Carcinoid syndrome Treatment
C Cost-limited resource
countries
Vitamin B3 replacement
D Disease (ie, Hartnup)

Bed rest and avoid sun
exposure

Ibuprofen is most common!
NSAID Toxicity
Early-Onset Symptoms Cardiovascular
Most have minimal
Abdominal pain, or no symptoms! Hypotension, shock,
nausea, vomiting bradyarrhythmia (in
Metabolic severe cases)
Central Nervous System Hyperkalemia, Gastrointestinal and Renal

hypocalcemia,
Headache, nystagmus, hypomagnesemia, Continued abdominal pain,
diplopia, altered mental metabolic nausea, vomiting, hepatic
status, coma, muscle acidosis injury, pancreatitis (rare),
twitching, and seizures acute kidney injury, upper
GI bleeding
Diagnosis and Workup Management
Diagnosis is mostly clinical—a thorough

history is needed
For ibuprofen, is the amount ingested...
<100 mg/kg?
Unlikely to result in toxicity
>400 mg/kg?
Toxicity is likely
Consider screening for potentially

dangerous coingestants
Acetaminophen level
Salicylate level
Obtain an ECG
Obtain a CBC and comprehensive
metabolic profile
Reproduced with permission from Tintinalli J, Stapczynski S, Ma OJ, et al:
Serum NSAID levels do not Tintinalli’s Emergency Medicine: A Comprehensive Study Guide,
8th ed. New York, NY: McGraw Hill; 2016.
correlate with toxicity or outcomes!

Another random document with
no related content on Scribd:
QUELQUES BANDITS
Nous sortions de la Renaissance, mon ami Cantarelli et moi.

Orso Cantarelli est un Corse d’Ajaccio plus qu’aménagé par dix ans
de séjour parisien et aussi répandu dans la politique que dans la
littérature ; le succès de l’Adversaire se reflétait dans ses yeux, la
solidarité corse atteint à l’intensité et à la force d’une franc-
maçonnerie, et ce soir-là, tout vibrant encore de la scène finale entre
Guitry et Brandes, Orso Cantarelli triomphait dans Emmanuel Arène.
J’éprouvai le désir de doucher cet enthousiasme.
— Ah ! ces Corses, lui disais-je en l’installant devant une
douzaine de natives, quels admirables conquérants, nés pour
l’intrigue et l’aventure, et quels dons de séduction ! Ce sont les
derniers conquistadors ou condottieri. Voyez, ce siècle appartient à
la Corse : Napoléon a conquis l’Europe et Emmanuel Arène vient de
dompter Paris. Et forçant sur l’ironie pour exaspérer le légendaire
orgueil de la race : D’abord vous êtes un pays de bandits.
Cantarelli haussa les épaules.
— Vous croyez encore que nous avons gardé le culte des
bandits ? Quel littérateur vous faites ! Le succès d’Arène vous gêne,
il vous gênerait échu à n’importe qui, mais vraiment vous avez perdu
votre temps, les deux mois passés, cet été en Corse, et vous croyez
encore à notre enthousiasme pour ces malheureux proscrits. C’est
une pitié et un bluff. Écoutez-moi, je suis bon prince :
« Nos bandits ! Vous avez, comme tous les continentaux, donné
dans le piège du décor. Les bandits ! C’est le cadre de montagnes et
de forêts qui les idéalise, la distance aussi, car ils sont si loin de
vous par la race et les habitudes ! La plupart enfin bénéficient à vos
yeux du recul du temps. Morts ou retirés dans les petits villages du
cœur de la Corse, ils vous apparaissent, dans les récits des
paysans, comme des héros de la légende ; ce sont les princes
lointains du maquis. Si l’on vous en montre un patriarche comme
Antoine Bellacoscia, nimbé de cheveux blancs, de petits-enfants et
de souvenirs, et, grangrené de romantisme comme vous l’êtes, vous
le prenez pour un personnage de la Bible. » Et Orso Cantarelli
m’enveloppait de la raillerie de ses yeux clairs ; puis, tout en tirant
une bouffée de fumée d’un gros cigare de son pays :
« Il faut donc en découdre de vos enthousiasmes, cher ami, et
surtout ne pas propager cette opinion, que nous avons tous
l’admiration de nos bandits. C’est avec ces histoires-là que vous
nous faites la réputation de sauvages, et notre île finit par passer
pour un repaire. Je sais bien que ce banditisme avéré nous vaut,
l’hiver, la clientèle d’Allemandes sentimentales et de vieilles misses
anglaises, mais croyez que nous préférerions de beaucoup des
hiverneurs français ; mais tous se cantonnent dans la Riviera. Hors
Nice, Cannes et Monte-Carlo, pas de salut pour un Parisien ! Mais
revenons à nos bandits, quelques-uns sont de véritables sacripants ;
je vous en fais juge :
« En 1889, un nommé Rochini gagne le maquis et le tient
pendant quinze ans, terrorisant tout le pays, de Propriano à
Sartène ; savez-vous ce qu’avait fait Rochini ? Amoureux d’une
paysanne de son village et repoussé par elle (la fille avait un fiancé)
Rochini déclarait à la malheureuse qu’il les tuerait, elle et l’homme
de son choix, si elle ne consentait pas à le suivre et à l’épouser. La
fille, en vraie Corse qui n’a qu’une parole, riait au nez de Rochini.
Celui-ci allait l’attendre à la fontaine — la fontaine où tout le village
corse se rencontre, s’aborde et s’entretient — s’arrangeait pour l’y
trouver seule, la mettait encore une fois en demeure de choisir entre
lui et son fiancé et, sur son refus, l’étourdissait d’un coup de crosse
de fusil et lui coupait les seins. Deux jours après, le fiancé de la
misérable fille recevait deux balles dans la tête. Un Apache de
Belleville n’eût pas fait mieux. Là-dessus Rochini prenait le maquis
et le tenait pendant quinze ans. Voilà ! Ne trouvez-vous pas un tel
personnage bien intéressant ?
« D’ailleurs il ne faut pas croire que le village et la montagne
tiennent en grande estime leurs bandits. Ils les subissent, terrorisés
par les représailles toujours menaçantes de ces « outlaws ». Le
paysan corse déteste le gendarme, mais a encore plus peur du
bandit. Une fois qu’il a gagné le maquis, le bandit s’érige de lui-
même en espèce de persona sacra. En même temps qu’il s’arroge le
droit de tirer au jugé et au visé sur tout porteur d’uniforme, il prélève
la dîme sur le paysan, il s’installe à son foyer, s’assied à sa table,
réclame le souper et le gîte et, quelquefois, la femme de son hôte.
Avec cela, horriblement méfiant (car ses méfaits ont mis sa tête à
prix et dans ce pays pauvre, la prime toujours assez forte peut tenter
les consciences) le bandit, toujours sur l’œil, craint l’embuscade, la
surprise et la trahison ; il entre chez le paysan en le mettant en joue
et exige, à l’heure des repas, que son hôte goûte avant lui de tous
les plats. Cette complicité, supportée comme un joug, amène
fatalement de brusques révoltes ; en tuant ou en livrant le bandit, le
paysan alors se venge des vexations subies, et c’est la mort de
Feretti, le bandit de Propriano.
« Poursuivi par les gendarmes, il s’était réfugié chez un sien
parent, lequel habitait une masure assez isolée dans la montagne. Il
s’y était installé comme chez lui, y commandait en maître, mettant la
main au plat et même aux corsages des filles. Il avait fait de celle de
son hôte, sa maîtresse, le père, dompté par la terreur, n’osait rien
contre le mécréant. Feretti plein d’une juste méfiance pour l’homme
qu’il terrorisait, lui faisait manger, avant et devant lui, de tous les
plats qui lui étaient servis. Le paysan eut une idée géniale : il trouva
le moyen d’introduire de la strychnine dans des figues fraîches, il en
avait délicatement coupé la queue. Les fruits empoisonnés furent
mêlés à d’autres, intacts : « Mange », faisait Peretti à son parent. Le
paysan s’exécutait. Il reconnaissait les figues. Rassuré, le bandit
puisait à l’assiette. A la quatrième figue il tombait foudroyé ; le
paysan s’était délivré de son oppresseur.
« Parfois, c’est l’appât du gain qui décide de la mort du bandit. La
prime a tenté le paysan, et dans ce cas-là, c’est presque toujours un
parent du bandit ou un de ses guides qui fait le coup, car le bandit
ne marche que précédé ou escorté d’un guide et, parfois, de
plusieurs, qui font autour de lui un vrai service d’avant-garde. Ils
explorent le pays, s’assurent de la sécurité du village où le proscrit
doit passer, préparent son gîte et favorisent sa fuite en cas d’alerte.
Comme les Chouans de Vendée, ils ont entre eux des signes d’eux
seuls connus ; trois pierres posées sur le bord de la route, à l’entrée
d’un village, préviennent le bandit de ne pas aller plus loin, le lieu
n’est pas sûr pour lui ; telle ou telle entaille dans un tronc de
châtaignier veut dire que les gendarmes vont passer par là et qu’il
doit bifurquer au plus vite à droite ou à gauche pour ne pas tomber
entre leurs mains ; et dans toute la contrée, l’arbre et la roche
deviennent complices pour protéger et sauver le bandit… Quand
l’homme dont la tête est mise à prix se dérobe, le paysan qu’a tenté
la prime s’avise quelquefois d’étranges supercheries ; ce fut le cas
d’un des neveux de Jacques Bellacoscia.
« Il rêvait depuis longtemps de gagner la grosse somme. La mort
de son terrible oncle pouvait seule la lui fournir ; mais, outre que
Jacques Bellacoscia n’était pas facile à surprendre, même par un
des siens, ce neveu intéressé redoutait les représailles de la famille.
Antoine Bellacoscia n’était pas homme à laisser le meurtre de son
frère impuni, et puis, tous les Bonelli auraient pris les armes, c’était
du coup tous les Bellacoscia dans le maquis.
« Ce madré neveu se décida pour un bandit moins proche, un
bandit qui ne fût pas de la famille.
« Un nommé Capa tenait alors la montagne entre Vivario et
Vizzavona, c’était un fin limier qui avait toujours déjoué les marches
et les contremarches de la maréchaussée et dont, chargée de
méfaits, la tête était chèrement cotée. Le neveu de Bellacoscia se
rabattit donc sur Capa, mais Capa n’était pas non plus homme à se
laisser approcher et abattre comme un vulgaire gibier. Après trois
mois de poursuites et d’embuscades, le malheureux coureur de
prime devait renoncer à tuer le fameux bandit, mais il ne renonçait
pas à la somme.
« Dans la légitime appréhension du fusil et des balles de Capa, il
se décida à une substitution ; le tout était de se procurer un cadavre
et de le fournir à la gendarmerie comme celui d’un bandit. Un
malheureux mendiant porteur de saintes images, un vieux
pellegrine, comme on les appelle ici, fut guetté et assassiné par le
paysan dans un sentier de forêt. La Corse est infestée de ces vieux
montreurs de saints, la plupart Italiens de naissance et qui,
loqueteux et chenus, s’en vont de village en village faire baiser aux
paysans la figure de cuivre ou d’étain repoussé, qu’ils portent
religieusement pendue à leur cou. Ceux-là sont sans défense, sans
famille aussi, et leur meurtre est facile. Un carrefour de forêt vit le
crime. L’homme abattu, l’assassin s’empressait de le défigurer, il lui
brûlait avec de la poudre la barbe et le visage. Le cadavre ainsi
rendu méconnaissable, le chasseur de prime courait prévenir la
gendarmerie, l’amenait sur les lieux, et lui faisait reconnaître le mort.
« — C’est Capa, je l’ai guetté, suivi et puis je l’ai tué ! J’ai bien
visé, voyez plutôt, à la tête.
« La maréchaussée mystifiée donnait dans le piège, un procès-
verbal constatait la mort du fameux Capa, le meurtrier touchait la
prime et vivrait encore heureux de polenta de châtaigne en hiver et
de polenta de maïs en été, si Capa, furieux de passer pour mort de
son vivant, n’avait réclamé.
« Il écrivit au préfet, au procureur de la République, aux
directeurs de journaux même, pour démentir sa mort et bien établir
qu’il était en vie ; il remua autour de la supercherie, qui le rayait du
nombre des Corses, l’opinion publique et la presse. L’assassin du
faux Capa était arrêté, une enquête était ouverte qui prouvait son
crime, l’identité du pauvre pellegrine était retrouvée et le Corse
amateur de primes passait en Cour d’assises et payait sa
substitution de cadavre de sa tête.
« Il fut guillotiné à Bastia,
« L’affaire et la mort du fameux bandit Poli, sa rencontre et ses
démêlés avec le préfet d’Ajaccio dans la forêt d’Aïtone, la victoria du
préfet arrêtée avec son escorte officielle par Poli et ses guides, et les
conditions du bandit imposées à l’officier ministériel couché en joue
pendant tout l’entretien, toute cette aventure détachée, on dirait des
Brigands d’Offenbach, a défrayé trop récemment l’opinion et la
presse pour y revenir. Poli, véritable brigand bien plus que bandit,
avait été trouver son oncle Lecca et essayé de le rançonner sous
menace de mort.
« Reçu à coups de fusil par Lecca, Poli avait juré de se venger et,
à quelque temps de là, en effet, Lecca avait été trouvé tué. Poli avait
alors gagné le maquis. Arrêté, puis condamné par la Cour de Bastia,
il avait été expédié en Nouvelle-Calédonie. Il était parvenu à s’en
échapper, s’était réfugié en Italie et, incarcéré à Rome comme
anarchiste, y avait toujours caché son identité et son nom. En Corse,
on le croyait mort.
« L’arrestation de ses deux frères, impliqués dans l’assassinat de
Lecca et emprisonnés comme complices, le ramenait au pays. En
apprenant que ses frères étaient compromis à cause de lui et par lui,
Poli, bravant tous les périls, rentrait en Corse. Il y affirmait sa
présence par des meurtres, des violences et des rapines, mettait le
pays en coupe réglée et de brigandage en brigandage, d’audaces en
audaces arrêtait la victoria du préfet et mettait ce dernier en
demeure de faire acquitter ses frères, alors sur le banc des Assises
de Bastia : « Ils étaient innocents, lui seul était coupable et se faisait
gloire de le proclamer. » « Le préfet promettait tout ce qu’exigeait le
bandit : les frères de Poli sortirent acquittés des Assises, mais la
nouvelle de la rentrée du meurtrier en Corse y avait ramené les fils
de Lecca, l’oncle assassiné. Pour venger leur père les trois fils
Lecca, l’un employé de chemin de fer sur le continent, l’autre sous-
officier en Tunisie et le troisième établi à Bône, en Algérie,
obtenaient des congés, se faisaient libres et, rentrés dans l’île, y
gagnaient le maquis.
« Ils y organisaient la chasse au bandit. Poursuivi par ses
cousins, traqué par les gendarmes, Poli était ramassé un matin en
forêt, mort à son tour. Un de ses guides l’avait empoisonné pour
toucher la prime.
« Pour une vendetta corse, en voilà une qui, à mon avis, vaut
bien celle de Colomba et pourrait tenter un moderne Mérimée, et
Poli a été tué, il y a six mois à peine.
« Les légendaires exploits des deux Bellacoscia deviennent bien
pâles dans le recul du temps auprès du sang tiède et fraîchement
versé de la querelle Lecca-Poli, et puis Antoine Bellacoscia a bien
perdu de son prestige depuis que les autorités de l’île l’ont classé
bandit décoratif dans les fêtes officielles ! Au dernier voyage de M.
Lockroy en Corse, une administration trop zélée n’a-t-elle pas eu
l’idée de camper le vieux Bellacoscia en costume de bandit sur
l’affreuse glacière en béton qui déshonore la station de Vizzavona,
et de grouper autour de lui une vingtaine de vieux paysans guêtrés
de peaux et vêtus de velours noir, toute une figuration de bandits de
circonstance qui, à la descente du malheureux Lockroy du train,
saluèrent d’une brusque fusillade Son Excellence.
« Fusillade héroïque de la Navarraise presque !!
« M. Carré n’eût pas mieux fait. Couleur locale et cabotinage.
« Le préfet d’alors avait servi des bandits au ministre, les bandits
se sont revanchés des préfets dans Poli.
« Un mot de Bellacoscia pour finir, du vieil Antoine Bellacoscia,
de celui-là même qu’ont un peu démonétisé les cartolines et les
fêtes officielles. Il fleure une odeur sauvage de poudre et de maquis.
« On causait au village du nouvel uniforme des gendarmes,
Bellacoscia était présent et, comme on consultait son avis, le vieil
homme, clignant de l’œil sur la grenade de cuivre doré, qui met un
point brillant au-dessus de la visière du shako d’aujourd’hui : Che
bella mira ! se contentait-il de dire ! Quel beau point de mire ! et dans
sa voix tremblait comme un regret.
TABLE DES MATIÈRES
De Marseille à Ajaccio 5
Lui ! 19
Dimanche corse 32
Les Quais 38
Les Pélerinages 45
Fleurs d’exil 52
Les Voceri 59
Le seize août en Ajaccio 67
Sous les Châtaigniers 81
Le Village 95
Quelques Bandits 107
Mayenne, Imprimerie Ch. COLIN.

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The Infographic Guide To Medicine Neeral L Shah Full Chapter

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The Infographic Guide to Medicine

With my specialty training in gastroenterology and transplant hepatology, I set out to

Neeral L. Shah, M.D.

Book ISBN 978-1-260-45398-0

Book MHID 1-260-45398-7

This book was set in Minion Pro by KnowledgeWorks Global Ltd.

The production supervisor was Richard Ruzycka.

Project management was provided by Harleen Chopra, KnowledgeWorks Global Ltd.

The cover designer was W2 Design.

Respiratory distress may be caused by edema of the upper airway, aspiration

Diagnosis and Workup

Copyright © 2022 by McGraw Hill. 107

03_Emergency Medicine_p105-190.indd 107 01/09/21 4:52 PM

Periumbilical to RLQ Pain Ruptured AAA

Intra-abdominal Nonsurgical Extra-abdominal

Cholecystitis, Screens for Appendicitis, Consult with Surgical Subspecialty as

Copyright © 2022 by McGraw Hill. 108

03_Emergency Medicine_p105-190.indd 108 01/09/21 4:53 PM

Consider activated charcoal if If acetaminophen level = Possibly toxic per

If single, acute ingestion, use...

Serum If chronic ingestion, consider...

Nomogram cannot be used for Liver transplant may be needed

Acetaminophen level >150 mcg/mL at Survivors of acetaminophen toxicity

Copyright © 2022 by McGraw Hill. 109

03_Emergency Medicine_p105-190.indd 109 01/09/21 4:53 PM

Fecalith (most common)

Generalized abdominal pain that

McBurney’s Point Diagnosis

Clinical diagnosis: Imaging for

Most patients require urgent

Copyright © 2022 by McGraw Hill. 110

03_Emergency Medicine_p105-190.indd 110 01/09/21 4:53 PM

Active and latent Clinical diagnosis based on

Altered mental status, Vitamin B6 (ie, pyridoxine)

Benzodiazepines may also be

Recurrent, refractory Supportive (ie, airway

Copyright © 2022 by McGraw Hill. 111

03_Emergency Medicine_p105-190.indd 111 01/09/21 4:53 PM

Significant global impact

Increased GABA activity and decreased Oxidation follows zero-order kinetics

Copyright © 2022 by McGraw Hill. 112

03_Emergency Medicine_p105-190.indd 112 01/09/21 4:53 PM

Mild Withdrawal Alcoholic Hallucinations

3-36 hours (after last drink) 12-48 hours

Delirium Tremens Management

2-7 days EtOH & benzos activate GABA receptors

Copyright © 2022 by McGraw Hill. 113

03_Emergency Medicine_p105-190.indd 113 01/09/21 4:53 PM

Copyright © 2022 by McGraw Hill. 114

03_Emergency Medicine_p105-190.indd 114 01/09/21 4:53 PM

Class II Class III Class IV

Clinical presentation: Clinical presentation:

*Supportive care (required by all):

Copyright © 2022 by McGraw Hill. 115

03_Emergency Medicine_p105-190.indd 115 01/09/21 4:53 PM

Medications (ie, antihistamines, atropine); Mushrooms; Plants

Tachycardia "Red as a beet" "Dry as a bone"

"Hot as a hare" "Blind as a bat" "Mad as a hatter" "Full as a flask"

Evaluation & Management

Flushing, anhidrosis, hyperthermia, blurry vision (mydriasis),

2 Perform basic screening tests Diagnosis is based on clinical findings

Fingerstick glucose—to rule out hypoglycemia

3 Manage anticholinergic toxicity

Preload CO Afterload