Fever and Cold (Upper Respiratory Tract Infection) in Children

Overview

• Tintinalli's Emergency Medicine, p. 788
• Harrison's Principles of Internal Medicine 22E, p. 297

1. What Is Fever?

• Any temperature above normal is considered a fever.
• In infants, the classic threshold of concern is 38°C (100.4°F) rectally.
• In neonates/infants <2-3 months, hypothermia (<36°C / 96.8°F) is equally alarming.
• Historically, fever >39°C (102.2°F) in children aged 3-36 months raises concern for occult bacteremia.
• Axillary temperatures run ~0.6°C lower than oral, which run ~0.6°C lower than rectal.

Note on moderate fever: Moderate fever is not always harmful - it is associated with decreased microbial reproduction and an enhanced immune response. Temperatures below 39°C in a healthy, comfortable child generally do not require drug treatment.

2. Common Cold (Nonspecific URI) - Causes

• Rhinoviruses (100+ serotypes) - most common
• Coronaviruses
• Parainfluenza virus
• Respiratory syncytial virus (RSV)
• Influenza virus
• Adenovirus
• Metapneumovirus

• Harrison's Principles of Internal Medicine 22E

3. Symptoms

• Nasal fullness, congestion, rhinorrhea (runny nose)
• Sore throat, laryngitis
• Low-grade fever
• Cough
• Lymphadenopathy
• Possible mild myalgias (muscle aches)

4. Management

A. Fever Treatment

• Aspirin is CONTRAINDICATED in children with viral URIs - it is associated with Reye syndrome (a rare but serious liver and brain condition).
• Do not alternate acetaminophen and ibuprofen - current evidence shows no benefit and it may be unsafe.
• Tepid sponge bathing is helpful as a supportive measure when used alongside antipyretic therapy.
• Tintinalli's Emergency Medicine, p. 788-789
• Swanson's Family Medicine Review

B. Nasal Congestion (Cold Symptoms)

Caution: Bulb suctioning done too frequently can cause nasal trauma, mucosal swelling, and worsening congestion.

C. Drugs to AVOID in Young Children

For older children and adolescents, adult-style symptomatic treatment (acetaminophen/NSAIDs for fever, ibuprofen for sore throat, oxymetazoline nasal spray for congestion, dextromethorphan for cough) may be considered.

• Swanson's Family Medicine Review, p. 549-550
• Harrison's Principles of Internal Medicine 22E

D. Antibiotics

5. Red Flags - When to Seek Urgent Care

• Fever >39°C (102.2°F) in a young child, or any fever in a neonate (<1 month)
• Fever lasting >5 days without an obvious source
• Rash with fever (especially petechiae or purpura - possible meningococcemia)
• Stiff neck or bulging fontanelle (possible meningitis)
• Shortness of breath or labored breathing
• Chest pain
• Lethargy, confusion, or the child appears "very ill"
• New ear pain or sinus pain (possible otitis media or sinusitis)
• Symptoms lasting >14 days
• Febrile seizure

6. Age-Specific Considerations

7. Complications to Watch For

• Otitis media - ear pain, irritability, tugging at ear
• Bacterial sinusitis - persistent purulent nasal discharge >10-14 days with facial pain
• Pneumonia - cough + fever + respiratory distress
• Meningitis - fever + stiff neck + photophobia + rash
• Kawasaki disease - fever >5 days with strawberry tongue, conjunctivitis, cracked lips, rash, lymphadenopathy (especially in children <5 years; requires aspirin + IV immunoglobulin)

Summary Table: Management at a Glance

Hypothermia in a 6-Year-Old Child - Emergency Medicine

Definition and Why Children Are at Higher Risk

• Higher body surface-area-to-mass ratio compared to adults = faster heat loss
• Less subcutaneous fat (insulation)
• Limited capacity for sustained shivering thermogenesis
• Children classified as "age extremes" are a mandatory indication for active rewarming

Harrison's Principles of Internal Medicine 22E documents the lowest recorded core temperature with successful resuscitation in a child: 11.8°C in a 2-year-old - demonstrating that profound hypothermia can be survived with aggressive management.

Classification by Severity

ECG Finding: The Osborn (J) Wave

Emergency Management

Step 1 - Immediate ABC + Stop Heat Loss

• Remove wet/cold clothing immediately
• Dry the child and cover with blankets (including the head - covers ~40% heat loss)
• Move to a warm environment (ambient temp >21°C / 69.8°F)
• Continuous cardiac monitoring (VF risk)
• Core temperature measurement (rectal or esophageal - peripheral thermometers are unreliable)
• IV access; draw labs (CBC, glucose, electrolytes, ABG, coagulation)

Step 2 - Assess Perfusion Status

• Do NOT assume death - in hypothermia, pulses may be undetectable even in perfusing patients; palpate for a full 60 seconds or use bedside echocardiography / ETCO2
• If no signs of life → begin CPR (see cardiac arrest section below)
• Do not withhold CPR based on temperature alone: "No one is dead until they are warm and dead"

Step 3 - Rewarming Strategy

Passive External Rewarming (PER)

• Insulate child in warm environment; cover entire body including head
• Rate: 0.5-2°C per hour
• Appropriate only for: mild hypothermia (>32°C), previously healthy child, able to shiver, no cardiovascular instability

Active External Rewarming (AER)

• Cardiovascular instability
• Core temperature <32°C
• Inadequate rate of passive rewarming
• Age extremes (children are explicitly listed)
• Endocrine insufficiency
• Trauma or secondary hypothermia

Critical warning: Do NOT apply heat to extremities in chronic/severe hypothermia - this causes peripheral vasodilation, sends cold blood to the core, and causes core temperature afterdrop (continued drop in core temperature after removal from cold). Apply heat to the truncal region only.

Active Core Rewarming (ACR)

Rosen's Emergency Medicine states: "Aggressive treatment of hypothermia is indicated in infants [and children]. Rapid rewarming is advantageous because it minimizes energy expenditure." A neonate with core temp 14.8°C and in CPR made a full neurologic recovery after active external rewarming + warmed IV fluids + heated humidified ventilator gases.

Step 4 - Cardiac Arrest Protocol in Hypothermia

• The 2025 AHA Guidelines for CPR and Emergency Cardiovascular Care (PMID 41122889) include specific guidance for hypothermic cardiac arrest in children alongside adults.
• ECMO is preferred for refractory hypothermic cardiac arrest when available.

Lab and Monitoring Pitfalls (Critical Pearls)

Causes to Consider in a 6-Year-Old

• Cold exposure (environmental - most common)
• Near-drowning (cold water submersion)
• Sepsis (infection impairs thermoregulation)
• Hypoglycemia or malnutrition
• CNS injury (head trauma, seizure)
• Toxicological (drug ingestion - alcohol, sedatives, opioids)
• Endocrine (hypothyroidism, adrenal insufficiency - rare at 6 years but possible)

Summary: Emergency Management at a Glance

HYPOTHERMIA IN A 6-YEAR-OLD
         │
         ▼
1. Remove cold/wet clothing. Dry. Cover (including head).
   → IV access, glucose check, cardiac monitor, core temp
         │
         ▼
2. Is there a pulse? (Check 60 seconds or use ECHO)
   ├── YES → Go to rewarming
   └── NO  → Start CPR immediately. Do NOT stop.
         │
         ▼
3. Rewarming (children = age extreme = ACTIVE required)
   Mild (>32°C, stable):  Passive + heated humidified O2
   Moderate (<32°C):      AER (forced air blanket, trunk) + heated O2 + warm IV fluids
   Severe (<28°C, VF):    Active core rewarming + ECMO if available
         │
         ▼
4. Defibrillate only if core temp >28°C
   (or after rewarming to ≥30°C)
         │
         ▼
5. Treat precipitating cause
   Glucose, antibiotics (if sepsis), toxicology screen

Hydrocortisone in Hypothermia - When, Why, and How

Direct Answer

Situation 1 - Secondary Hypothermia from Adrenal Insufficiency

• Thermogenesis is impaired
• The stress response to cold fails
• The patient cannot mount normal cardiovascular and metabolic compensation

Key Clinical Clue: Failure to Rewarm

"Although failure to rewarm spontaneously has been noted in victims with hypothyroidism and other endocrine deficiencies, reserve the use of thyroid hormones and corticosteroids for patients with suspected thyroid and adrenal insufficiency, respectively."

Situation 2 - Myxedema Crisis with Hypothermia

1. Severe hypothyroidism is commonly associated with concurrent adrenal insufficiency
2. Starting thyroid hormone replacement without covering adrenal function can precipitate acute adrenal crisis (by accelerating cortisol metabolism before the adrenal glands can compensate)
3. Hydrocortisone prevents this adrenal crisis and also supports hemodynamic stability

Dosing in Myxedema Crisis (from Tintinalli's Emergency Medicine)

"For myxedema crisis, give a stress dose of hydrocortisone (100 to 200 milligrams IV) at the start of therapy. Obtain serum cortisol levels prior to initiation of therapy, but it is not necessary to wait for results."

• Tintinalli's Emergency Medicine

"Hydrocortisone (50 mg every 6 hours until adrenal insufficiency is excluded) are usually added prior to starting L-thyroxine because of the concern of associated adrenal insufficiency."

Why NOT Routine Hydrocortisone for All Hypothermia?

Practical Algorithm for Hydrocortisone Decision in a Hypothermic 6-Year-Old

Is the child failing to rewarm despite good technique?
         │
         ├── NO → Continue standard rewarming. No steroids.
         │
         └── YES → Consider secondary hypothermia
                        │
                        ├── Evidence of hypothyroidism?
                        │   (bradycardia, puffy face, dry skin,
                        │    delayed relaxation of reflexes, low T4/TSH)
                        │       └── YES → Myxedema crisis
                        │                 Give Hydrocortisone 100-200 mg IV FIRST
                        │                 Then add thyroid hormone replacement
                        │
                        ├── Evidence of adrenal crisis?
                        │   (refractory hypotension, hyponatremia,
                        │    hyperkalemia, hypoglycemia, skin pigmentation)
                        │       └── YES → Give Hydrocortisone 50-100 mg IV
                        │                 (stress dosing)
                        │
                        └── Neither suspected → Standard rewarming +
                                                treat other causes
                                                (sepsis, toxins, CNS injury)

Important Note for a 6-Year-Old Specifically

• Congenital adrenal hyperplasia (CAH) - inadequately treated
• Autoimmune adrenal insufficiency (Addison's disease in older children)
• Long-term steroid use followed by sudden withdrawal (relative AI)
• Panhypopituitarism (from CNS tumor, craniopharyngioma, or trauma)
• Hypothyroidism (acquired autoimmune or untreated congenital)

Summary

Bottom line: Hydrocortisone treats the endocrine cause of hypothermia, not the hypothermia itself. The treatment of hypothermia is rewarming.

Hydrocortisone After TKR/THR - The Clinical Reasoning

The Post-Arthroplasty Triad: What Causes It?

1. Fat Embolism Syndrome (FES) - The Most Likely Culprit

What Happens in TKR/THR?

• Lodge in the pulmonary microvasculature → mechanical obstruction → hypoxia, low SpO2
• Trigger free fatty acid release → toxic damage to capillary-alveolar membrane → ARDS
• Release vasoactive amines and prostaglandins → systemic inflammatory response → fever
• Can cross to the systemic circulation (through a patent foramen ovale) → cerebral involvement

Classic Triad of FES (Gurd's Criteria)

1. Respiratory - hypoxemia, low SpO2, ARDS pattern on chest X-ray (bilateral diffuse infiltrates)
2. Neurological - confusion, restlessness, deteriorating consciousness
3. Petechial rash - conjunctiva, axillae, neck skin folds (pathognomonic)

Role of Hydrocortisone / Corticosteroids in FES

"There is currently no evidence supporting the use of steroids, heparin, or dextran in the management of FES."

• Miller's Anesthesia 10e

"The use of corticosteroid therapy in preventing or treating fat embolism syndrome is controversial."

• Morgan and Mikhail's Clinical Anesthesiology 7e

• FES involves a massive systemic inflammatory response mediated by free fatty acids, prostaglandins, and vasoactive amines
• Corticosteroids are potent anti-inflammatory and membrane-stabilizing agents
• They reduce capillary leak, attenuate the inflammatory cascade, and may reduce pulmonary edema
• Some older studies showed prophylactic methylprednisolone reduced FES incidence after long bone fractures
• In clinical practice, when a patient is deteriorating rapidly with FES, hydrocortisone is often given empirically as a "stabilizing" measure while definitive support (oxygen, ventilation) is established

2. Bone Cement Implantation Syndrome (BCIS) - The Intraoperative/Immediate Post-Op Cause

Mechanism

• Bone marrow debris, fat, and cement monomer are forced into the venous circulation
• Cause pulmonary embolization → right ventricular failure → hypotension, hypoxia, low SpO2
• Methyl methacrylate monomer is directly cardiotoxic → bradycardia, arrhythmias
• Release of cytokines and cyclooxygenase products → pulmonary vasoconstriction → bronchoconstriction

Management of BCIS (from Miller's Anesthesia 10e)

• 100% oxygen
• Fluid resuscitation
• Vasopressors (epinephrine is preferred to off-load the right ventricle)
• Mechanical ventilation if needed

1. The cytokine storm and COX-product release mimics an inflammatory/anaphylactoid reaction
2. Corticosteroids help blunt this inflammatory cascade
3. It is used alongside epinephrine in the management of anaphylactoid reactions to cement

3. Anaphylaxis/Anaphylactoid Reaction

• Bone cement (methyl methacrylate) - anaphylactoid (non-IgE mediated)
• Prophylactic antibiotics (cefazolin, vancomycin) - true anaphylaxis
• Latex (gloves, tourniquet components)
• Blood products (if transfused)

Classic Anaphylaxis Triad After Surgery

• Hypotension (vasodilation)
• Bronchospasm → low SpO2
• Urticaria/rash (may be missed under surgical drapes)
• Fever can occur in anaphylactoid reactions

Hydrocortisone Dosing in Anaphylaxis - Well-Established Indication

Important: In anaphylaxis, hydrocortisone does NOT act fast enough to treat the acute attack - it takes 4-6 hours to work. Its role is to prevent a biphasic (second-wave) reaction 4-12 hours later. Epinephrine always comes first.

4. Post-Operative SIRS (Systemic Inflammatory Response Syndrome)

• TNF-alpha, IL-1, IL-6 surge in the first 24-48 hours
• This causes: fever, tachycardia, mild hypoxia (from microatelectasis)
• Rarely causes significant bradycardia

Summary: Why Doctors Give Hydrocortisone After TKR/THR

The Honest Bottom Line

1. Empirical anti-inflammatory management in a deteriorating patient
2. Rational based on the known mechanism (inflammatory cascade)
3. Low-risk relative to the severity of the situation
4. Practiced widely despite limited hard evidence

Gentamicin - Complete Clinical Guide

What Is It?

Mechanism of Action

1. Enters the bacterial cell - transported across the bacterial cell membrane via an oxygen-dependent active transport system (this is why it is ineffective against anaerobes - no oxygen, no entry)
2. Binds irreversibly to the 30S ribosomal subunit - causes misreading of mRNA codon → production of faulty/nonsense proteins → insertion of wrong amino acids → abnormal proteins disrupt the cell membrane → increased permeability → more drug enters → cell death

Antibacterial Spectrum

Clinical Uses - Where Is Gentamicin Used?

1. Serious Gram-Negative Infections (IV/IM - Main Use)

• Sepsis / bacteremia from gram-negative organisms
• Hospital-acquired (nosocomial) pneumonia - Pseudomonas, Enterobacter, Klebsiella (but NOT as single agent - poor lung penetration due to low pH and oxygen tension in infected lung)
• Complicated urinary tract infections (pyelonephritis, urosepsis) - excreted in urine at high concentrations
• Peritonitis / intraabdominal sepsis - combined with metronidazole for anaerobic cover
• Meningitis from gram-negative organisms (when beta-lactams fail)
• Osteomyelitis and septic arthritis caused by gram-negative organisms
• Neonatal sepsis - a key empiric drug in combination (ampicillin + gentamicin)
• Febrile neutropenia - empiric cover in immunocompromised patients

2. Endocarditis (Synergistic Use) - Gram-Positive Cover

Mechanism: Cell wall agents (penicillin, vancomycin) create pores in the gram-positive cell wall, allowing gentamicin to enter (normally excluded) → synergistic bactericidal killing. This synergy is the reason gentamicin is used even against organisms that seem "resistant" to it alone.

Important: For synergistic dosing in endocarditis, target peak 3-4 mcg/mL, much lower than standard dosing (peak 6-10 mcg/mL).

3. Topical Use

• Infected wounds, burns, ulcers - 0.1% cream or ointment
• Eye infections (conjunctivitis, keratitis, blepharitis) - 0.3% ophthalmic drops or ointment
• Intravitreal injection - for serious bacterial endophthalmitis

4. Intrathecal/Intraventricular (Rare)

• Gram-negative meningitis refractory to beta-lactams or severe beta-lactam allergy
• Largely replaced by 3rd-generation cephalosporins

5. Intratympanic Injection - Special Use in ENT

• Ménière's disease - intratympanic gentamicin selectively destroys vestibular hair cells to ablate the labyrinthine function on the affected side, reducing vertigo attacks
• This is a deliberate ototoxic effect used therapeutically

Dosing (Important Concepts)

Once-Daily (Extended-Interval) vs. Divided Dosing

Pediatric Dosing (Harriet Lane Handbook)

• Children (eGFR >75 mL/min/1.73m²): 7.5 mg/kg/24h divided q8h
• Neonates: dose by postconceptional age (see neonatal table - 4-5 mg/kg q24-48h)
• Cystic fibrosis: 7.5-10.5 mg/kg/24h (higher clearance requires higher dose)

Therapeutic Drug Monitoring (TDM) - Mandatory

Toxicities - The Critical Dangers

1. Nephrotoxicity (Kidney Damage)

• Occurs in 5-25% of patients receiving gentamicin >3-5 days
• Caused by accumulation in renal proximal tubule cells
• Presents as non-oliguric acute tubular necrosis (rising creatinine, falling urine output)
• Usually reversible on stopping the drug
• Risk factors: pre-existing renal disease, volume depletion, concurrent nephrotoxins (NSAIDs, vancomycin, contrast agents, amphotericin)

2. Ototoxicity (Ear Damage)

• Occurs in 1-5% of patients on gentamicin >5 days
• Often irreversible
• Manifests mainly as vestibular toxicity (dizziness, loss of balance, oscillopsia) - more common than cochlear
• Hearing loss (cochlear toxicity) also occurs
• Worsened by concurrent loop diuretics (furosemide) - avoid combination
• Partly genetically determined - linked to mitochondrial DNA mutations

3. Neuromuscular Blockade

• Rare but life-threatening
• Can cause respiratory paralysis - especially dangerous in patients on neuromuscular blocking agents (surgery) or those with myasthenia gravis
• Caution in patients receiving anesthetics or neuromuscular blockers

4. No activity in pregnancy (Category D for IV use) - avoid if possible

Contraindications and Cautions

Quick Summary Reference