Emergencies Flashcards
Case
1 year old female, from Tondo 10 kg
CC: high grade fever
HPI:
1 week PTA: Patient was noted to have swelling and redness of the back of her Left shoulder with associated undocumented
fever. Mother noted scratching and attributed it to a possible insect bite. She was given Paracetamol with noted lysis of fever.
She was then brought to the local hilot wherein an oil-based liniment was applied as well as leaves from an unknown plant.
2 days PTA: Patient was noted to have high grade fever and inconsolable crying with one episode of vomiting of previously ingested milk. Persistence of symptoms with associated weakness and poor appetite prompted consult at the emergency room.
CBC
done outside revealed Hgb 130 Hct 0.35 WBC 18,000 Neutr 0.88
Lym 0.11 Plt 190,000.
PMHx:
No history of asthma or allergies nor previous hospitalizations.
Noted history of scabies treated at the local health center around
3 months ago
FMHx:
(+) brother, 4 yrs old with impetigo over his R leg, with secondary
crusting and excoriations
(+) sister, died of severe dehydration due to AGE at 1 yr old
BMHx: Born full term, via spontaneous vaginal delivery at home,
c/o hilot
No fetomaternal complications
Immunization Hx: completed EPI. NO PCV , NO INFLUENZA
Nutritional Hx: presently eats regular table food comprising of rice
and fish. Milk supplementation with Nido.
Developmental Hx: head control at 3 months. Presently walks
with support. Able to say Mama
Social Hx: Youngest of six siblings. Mother is a fish vendor. Father
is a tricycle driver.
Physical Examination:
Awake, irritable, inconsolable crying Wt: 10 kg
HR 160’s RR 40 Temp 39.1 BP 80/50
Pink conjunctivae, anicteric sclera, no TPC
Equal chest expansion, clear BS< (-) rales/wheezes
Adynamic precordium, distinct heart sounds, tachycardic, no murmur
Soft, globular abdomen, normoactive bowel sounds, no hepatomegaly
Normal external genitalia
Full pulses, pink nailbeds, (+) soft erythematous raised plaque
over L shoulder with spread to the back, minimally fluctuant and tender
Cool extremities, with generalized flushing, CRT = 4 sec.
LABORATORY RESULTS
CBC: Hgb 134, Hct 0.36, WBC 16,000 Neut 0.88 Lym 0.16 Plt
160,000
CXR: normal
Urinalysis: normal
Blood Culture: MRSA, S: Vancomycin, Linezolid
Serum Procalcitonin: 15 ug/L
Serum Lactate: 8 mmol/L
ESR: elevated
Creatinine: normal
ASO: normal
ABG: pH 7.29 / pCO2 30 / HCO3 15 / pO2 188/ O2sats 99%
What are the differentials?
DIFFERENTIAL DIAGNOSES (fever with skin manifestation)
Allergic: Urticaria
Contact dermatitis
Anaphylaxis
Immune-mediated : Erythema nodosum
Infectious: Sepsis; Septic Shock
Staphylococcal Infection (cellulitis)
Streptococcal Infection (erysipelas)
Viral exanthems
Necrotizing fasciitis
Toxicologic: Chemical exposure (oil liniment)
DIAGNOSIS: MRSA Sepsis
in septic shock, secondary to Soft tissue infection (Cellulitis vs Abscess)
Animal bite
Management of this case
MANAGEMENT
I. Stabilize patient
a. Establish airway
b. Support breathing, oxygenation, ventilation
c. Maintain circulation – fluids, inotropes,
vasopressors
d. Goals during the first 6 hrs of resuscitation:
i. Central venous pressure 8– 12mm Hg
ii. Mean arterial pressure (MAP) ≥65mm Hg
iii. Urine output ≥ 0.5 mL/kg/hr
iv. Central venous (superior vena
cava) or mixed venous oxygen
saturation 70% or 65%,
respectively
v. In patients with elevated lactate
levels targeting resuscitation to
normalize lactate.
e. Frequent reassessment
II. Administer broad-spectrum antibiotics within 1st hour ideally after specimen for blood cultures are sent. (VANCOMYCIN)
III. Source control. Locate source of infection and remove, if possible. Refer to Surgery for possible debridement.
IV. Transfer to Pediatric ICU for close monitoring.
Referral to Pediatric Intensivist
V. Preventive Care
a. Immunization update
b. Counseling on nutrition, hygiene, sanitation,
toxic exposure, injury prevention
i. Advice mother to treat the
infection of his brother as well
c. Iron, Vitamin A supplementation
d. Deworming
e. Counseling on child maltreatment
CH 70: SHOCK
What is shock?
CH 70: SHOCK
Etiopatho
Shock – state in which the delivery of oxygen is inadequate to meet the metabolic demands of the vital organs and tissues
- All types of shock can lead to impaired functioning of vital organs such as the brain and kidneys
- Continued presence of trigger + body’s exaggerated and harmful neurohumoral, inflammatory, and cellular response leads to progression of shock
Multiple organ dysfunction syndrome (MODS) – usual cause of death. Any alteration of organ function that requires medical support for maintenance
What is warm shock?
Warm shock – in the early stages (hyperdynamic phase, low SVR) CO increases in an attempt to maintain adequate oxygen delivery and meet the greater metabolic demands of the organs and tissues
What is cold shock?
Cold shock – as shock progresses, CO falls in response to numerous inflammatory mediators, leading to a compensatory
elevation in SVR
Pathophysiology of shock
Insult –> shock –> inadequate oxygen delivery to organs and tissues –> compensatory mechanism to maintain BP: inc CO and SVR; to optimize oxygenation: inc oxygen extraction and BF
directed to brain, heart, and kidneys –> compensated shock –>
inadequate mgt –> decompensated shock –> MODS –> death
What are the types of shock?
Types of Shock
1. Hypovolemic shock
- MC cause of shock in children worldwide
- Etiology: massive losses from diarrhea, hemorrhage, burns, osmotic diuresis, inadequate fluid intake, nephrotic syndrome, vomiting
- CM: hx of fluid losses (GI, blood loss, burns, insensible losses)
- Physio: dec preload (due to ext or int losses) will lead to dec SV and CO
o compensatory mechanisms: inc contractility
and inc afterload
- Cardiogenic shock
- Etiology: CHD, arrhythmia, cardiomyopathy,
myocarditis, myocardial injury or trauma
- CM: signs of CHF (crackles, jugular venous distention, hepatomegaly), cyanosis
- Physio: cardiac pump failure (dec CO) due to abN cardiac function
o Compensatory mech: tachycardia and inc
afterload
o Pulmonary edema may occur - Obstructive shock
- Et: tension pneumothorax, pericardial tamponade, constriction of ductus arteriosus in infants with ductal dependent
lesions, pulmonary embolism. Any lesion
that creates a mechanical barrier that impedes adequate CO
- CM: hx of trauma, sudden DOB
- RF for pulmonary embolism: prolonged immobilization, malignancy, hypercoagulable states
- Physio: impaired blood flow (dec CO) due to limited venous return to the heart or limited pumping of blood from the heart leads to dec CO and a compensatory inc in SVR - Distributive shock
- Et: anaphylaxis, SC injury, drugs
- CM:
o Anaphylaxis: acute onset of hypotension,
often accompanied by wheals, angioedema,
pruritus, dyspnea, wheezing, abd pain,
vomiting, LOC
o SCI: hx of trauma, dysautonomia
- Physio: abN of vasomotor tone from loss of venous and arterial capacitance (maldistribution of fluid)
o Anaphylaxis: vasodilation, inc capillary
permeability, pulmonary vasoconstriction
lead to reduced CO
o SCI: loss of vascular tone leads to severe
vasodilation and hypotension - Septic shock
- Et: bacterial, viral, fungal infections
- CM: fever, tachycardia, tachypnea, leukocytosis, focus of infection
- Physio: encompasses multiple forms of shock
o Hypovolemic: third spacing of fluids into the
extracellular, interstitial space
o Distributive: early shock with dec afterload
o Cardiogenic: depression of myocardial
function by endotoxins
o high or low SVR that leads to maldistribution of blood flow
o Inc capillary permeability and dec cardiac
contractility
What is the pathophysiology of shock?
—–Extracorporeal fluid loss—–
-hypovolemic shock may be result of direct blood loss through hemorrhage or abnormal loss of body fluids (diarrhea, vomiting, burns, diabetes mellitus or insipidus, nephrosis)
—–Lowering plasma oncotic forces—–
-hypovolemic shock may also result from hypoprotenemia (liver injury, or as a progressivecomplication of increased capillary permeability)
—–abnormal vasodilation—–
distributive shock (neurogenic, anaphylaxis, or septic shock) occurs when there is loss of vascular tone- venous, arterial or both (sympathetic blockade, local substances affecting permeability, acidosis, drug effects, spinal cord transection)
—–Increased vascular permeability—–
sepsis may change the capillary permeability in the absence of any change in capillary hydrostatic pressure (endotoxins from sepsis, excess histamine release in anaphylaxis)
—–Cardiac dysfunction—–
peripheral hypoperfusion may result from any condition that affects the heart’s ability to pump blood efficiently (ischemia, acidosis, drugs, constrictive pericarditis, pancreatitis, sepsis)
Diagnosis of Shock
CBC: may be normal; leukocytosis or leukopenia, thrombocytopenia, anemia
Blood chem: Low K due to failure of the energy-dependent transport mechanism; increased lactate due to metabolic acidosis associated with tissue hypoxia and anaerobic metabolism (present in all forms of shock); renal dysfunction (elevated crea, BUN); hepatic dysfunction
ABG: hypoxemia, hypercarbia, acidosis
SCVO2 (central venous O2 saturation):
used to monitor adequacy of o2 delivery; normal value is 70-75% higher if atrterial O2 sat is 100%; about 25-30% below the arterial O2 sat if the arterial O2 sat is not normal
Hematologic abnormalities:
prolonged prothrombin and PTT; reduced serum fibrinogen level
Management of SHOCK
General approach to SHOCK
1. Positioning: responsive and stable child: put in the most comfortable position; hypotensive child: place the child in a supine position
- Support airway, oxygenation and ventilation: maintain patent airway, provide high concentration of O2 to all with shock via high flow delivery system (non-rebreather mask at 10LPM); oxygenation and ventilatory support for patients with ineffective respirations, altered sensorium or increased work of breathing
- Established vascualr access: for compensated shock–> peripheral vebous cannulation
for hypotensive shock: immediate vascular access through intraosseous route if peripheral access is NOT readily achieved - Provide Fluid resuscitation:
for hypovolemic shock: isotonic crystalloid solution (NS/LR) should be given as a 20mL/kg bolus over 5-20mins
*For suspected cardiogenic shock: smaller boluses of isotonic crystalloid fluid at 5-10ml/kg given over 10-20 mins
*For trauma and massive bleeding: give packed RBCs (10ml/kg) if the child does not respond to isotonic crystalloid
*For neurogenic, anaphylactic and obstructive shock: 20ml/kg isotonic crystalloid
*Reassess the ff: and repeat fluid boluses as needed: HR, CRT, UO, level of consciousness
*For most: fluid boluses can be administered up to over 60ml/kg
Monitor the px:
SpO2 and HR monitoring asap
mental status
temperature
ensure optimal UO (may insert indwelling urinary catheter): infants and children: 1.5-2ml/kg/hr; older child and adol: 1ml/kg/hr
ongoing fluid losses
manage hypoglycemia (<45 mg/dl for neonates and <60mg/dl for the rest); consider central venous or arterial catheterization
Pharmacologic management
vasoactive medications are indicated when shock persists despite adequate fluid resuscitation
INOTROPES:
Dopamine, Dobutamine, Epinephrine
*increases cardiac contractility, increases HR, variable effects on SVR
VASOPRESSORS:
Epinephrine, Norepinephrine, Dopamine, Vasopressin
*increases SVR, increases contraction of the myocardium (except vasopressin)
PHOSPHODIESTERASE INHIBITORS
Milrinone
decreases SVR, improves contractility, improves coronary artery blood flow
D. For Specific Types of Shock
- Obstructive shock from ductal-dependent lesions like LVOT obstruction: Prostaglandin E1
- Anaphylactic shock: epinephrine, antihistamine, shortacting B2 agonist, steroids
- Fluid refractory shock:
a. Reverse warm shock by NE –> Dopa
b. Reverse cold shock by E –> dopa - Catecholamine resistant shock: hydrocortisone
Pediatric Poisoning
Intentional poisonings (suicide attempts, abuse, or misuse) are
often more severe than unintentional, exploratory ingestions
Clinical manifestations of poisoning
CM
1. Hx: toddler or adolescent, acute onset of sx without prodrome, sudden alteration of mental status, multiple system organ dysfunction, household stress
- PE: key fx are VS, mental status, pupil size and reactivity, nystagmus, skin, bowel sounds, odors
Diagnostics of poisoning
Dx
1. Gas chromatography/ mass spectroscopy – gold standard. Confirmatory
2. E’s, BUN, crea, glu
3. Urine pregnancy test – mandatory for all adolescents
4. ECG
Management of poisoning
Mgt
Principle of mgt are supportive care, antidotes, decontamination,
and enhanced elimination
APPROACH TO THE POISONED PATIENT
APPROACH TO THE POISONED PATIENT
*Stabilization, ABC and GCS, laryngeal reflexes
*In any patient with altered mental status obtain serum dextrose concentration
*Consider naloxone administration
HISTORY
*Problem-oriented history
*Without witnessed exposure: age, acute onset of symptoms without prodrome, multisystem organ dysfunction, or high level of household stress suggest POISONING
*Witnessed exposure: determine exactly what the child was exposed to
*For household, workplace products: Names (brand, generic, chemical) and specific ingredients along with concentrations
* Poison center specialists can help identify the pills based on markings, colors and label
* If unknown pill: a list of all medications in the child’s environment must be obtained
*If unknown exposure: clarify where the child was found (ex. Kitchen, garage, laundry room, backyard, workplace)
*Clarify the timing of ingestion and obtain the estimate of how much was ingested
Symptoms:
*Description of symptoms after ingestion including timing of onset relative to time of ingestion
*Identify TOXIDROMES
Past Medical and Developmental History
*Underlying disease, concurrent drug therapy, history of psychiatric illness, pregnancy
*Developmental history: ensure that exposure history provided is appropriate for child’s developmental stage
Social History
*Identify potential sources of exposure (caregivers, visitors, grandparents, parties)
*Identify potential circumstances (new baby, illness in the family)
PHYSICAL EXAMINATION
*Targeted PE
*Airway, Breathing, Circulation, mental status
*Vital signs, mental status, pupils (size and reactivity), nystagmus, skin, bowel sounds, muscle tone
LABORATORY EVALUATION
*Basic chemistry panel (electrolytes, renal function, glucose) necessary
*Acidosis (low serum bicarbonate level) calculate anion gap
*Acetaminophen overdose: monitor AST/ALT, INR
*Urine pregnancy test mandatory for all postpubertal female patients
*Both the rapid urine drug-of-abuse screens and the more comprehensive drug screens vary widely in their ability to detect toxins and generally add little information to the clinical assessment
*ECG
oWidened QRS interval: monomorphic ventricular tachycardia blockade of fast sodium channels
oWidened QTc interval: risk for torsades de pointes
oChest Radiography: check for pneumonitis, pulmonary edema, foreign body
oAbdominal radiography: most helpful in lead paint chips, foreign body
PRINCIPLES OF MANAGEMENT
PRINCIPLES OF MANAGEMENT
* Supportive care, decontamination, directed therapy (antidote, ILE), enhanced elimination
* Contact Poison control center
* Supportive care
o ABCs; intubation of needed
o Tachypneic with clear lung examination acidemia
o Hypotensive patients often are not hypovolemic thus aggressive fluids may lead to overload
o Dysrhythmias standard manner
o Seizure manage with GABA complex
* Decontamination
o Should not be routinely employed for every poisoned patient
o Dermal and ocular decontamination: removal of contaminated clothing and particulate matter flushing of affected area with tepid water or normal saline (NS) for min of 10-20min or longer for some chemicals (alkaline corrosives)
o Dermal decontamination include cleansing with soap and water
o GI decontamination most likely effective in 1 or 2 hours after acute ingestion; GI decontamination >2hrs after ingestion may be considered in patients who ingest toxic substances; methods emesis with ipecac, gastric lavage, cathartics, activated charcoal and whole-bowel irrigation (WBI); of these only activated charcoal and WBI are of potential benefit
Syrup of Ipecac: 2 emetic alkaloids: CNS and locally in GI tract to produce vomiting; AAP in facvor of abandoning the use
Gastric lavage: time consuming and painful and can induce bradycardia; use no longer recommended
Single-Dose Activated Charcoal: useful method of GI decontamination; Charcoal activated by heating to extreme temp preventing absorption; most likely effective when given 1hr of ingestion; administration should be avoided after ingestion of caustic substance
* Dose of activated charcoal with or without sorbitol is 1g/kg in children or 50-100g in adolescents and adults
* Ensure patient’s airway is intact or protected and with benign abdominal examination
Cathartics: sorbitol, magnesium sulfate, magnesium citrate
Whole Bowel Irrigation: instill large volume (35ml/kg/hr in children or 1-2L/hr in adolescents) of PEG electrolyte solution
* Decontaminate the gut; never do to patients with sign of bowel obstruction or ileus
* Directed therapy
o Antidotal therapy
o Intralipid emulsion therapy: lifesaving intervention; sequesters fat-soluble drugs, decreasing impact at target organ
* Enhanced Elimination
o Urinary alkalinization: enhances elimination of drugs that are weak acids by forming charged molecules
Continuous infusion of sodium bicarbonate-containing IV fluids with a goal urine PH of 7.5-8
Most useful in managing salicylate and methotrexate toxicity
o Hemodialysis
Toxins amenable to dialysis: low volume of distribution (<1 L/kg) with high degree of water solubility, low molecular weight and low degree of protein binding
Methanol, ethylene glycol, salicylates, theophylline, bromide, lithium and valproic acid
o Multidose Activated Charcoal
0.5 g/kg every 4-6hrs (4 doses)
Recommended in managing ingestions of carbamazepine, dapsone, phenobarbital, quinine and theophylline
Assess airway and do abdominal examination before each dose
