Paediatrics (Y4) > Acute presentations > Flashcards

Acute presentations Flashcards

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1
Q

sepsis

A
  • Sepsis is a life-threatening illness caused by the body’s response to an infection.
  • Recognising sepsis is often very difficult in children as symptoms and signs can be similar to self- limiting or less severe conditions.
  • Bacterial infections are by far the commonest cause of sepsis (can be viral or fungal).
  • Sepsis is defined as suspected/proven infection with Systemic Inflammatory Response (SIRS).
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2
Q

presentation of sepsis

A

SIRS is the presence of at least 2 of the following:

One of which must be temperature or WCC

  • Core temperature > 38.5oC or < 36oC.
  • Tachycardia (in absence of external stimuli). Tachypnoea for age (or ventilation).
  • White cell count elevated or depressed
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3
Q

screening for sepsis

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4
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managment of sepsis

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5
Q

anaphylaxis

A
  • Severe, life-threatening allergic reaction that is acute in onset and can cause death.
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6
Q

differentials for anaphylaxis

A
  • Skin: Acute urticaria.
  • GUT: Food poisoning, gastroenteritis.
  • Respiratory: URTI, irritant rhino-conjunctivitis, choking, viral wheeze. acute asthma exacerbation.
  • CVS: vasovagal syncope, panic attack.
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7
Q

presentation of anaphylaxis

A
  • Angioedema same pathophysiology as urticaria, however occurs in deeper layer of the skin with no itch receptors therefore not itchy like acute urticaria
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8
Q

management of suspected anaphylaxis

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9
Q

classic history for acute urticaria

A
  • Woke this morning with rash:
  • Raised erythematous plaques.
  • Some have pale centre.
  • Rash spreading; plaques coalescing.
  • Rash intensely pruritic.
  • Agitated, irritable and unhappy.
  • No previous allergies; eats all foods.
  • No recent new contact – food, drug.
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10
Q

acute urticaria background

A
  • Also called hives, wheals or welts.
  • Common condition affecting up to 20% of population.
  • Typically intensely pruritic erythematous plaque.
  • May be associated with angioedema (swelling).
  • Commonly categorized by chronicity:
  • Acute: <6 weeks; triggers allergy, URTI, idiopathic.
  • Chronic: >6 weeks; spontaneous or physical triggers
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11
Q

presentation of acute urticaria

A

Presentation
- Intensely pruritic rash
- Agitated, irritable, unhappy
- Spreading rash
- Raised erythematous plaques

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12
Q

management of acute urticaria

A
  • History and examination to make diagnosis.
  • In new-onset acute urticaria where assessment does NOT suggest underlying cause, NO investigations; may consider FBC and CRP if worried about vasculitis.
  • High-dose non-sedating antihistamines.
  • ± Oral glucocorticosteroids.
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13
Q

paracetamol overdose protocol overview 1/2

A
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14
Q

history for paracetamol overdose

A

o Dose
o Timing
o Associated ingestions

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15
Q

paracetamol overdose protocol overview 2/2

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16
Q

management of paractermaol overdose

A

charcoal only if very recently ingested

defintive treatment: N-acetylcysteine infusion

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17
Q

differential diagnosis

A

* Pre-septal cellulitis.
* Orbital or Post-septal cellulitis. * Allergicconjunctivitis.
* Bacterial conjunctivitis.
* Trauma.
* Sub-periostal/orbital abscess. * Cavernous sinus thrombosis.

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18
Q

history and examiantion for red swollen eye

A
  • Acuity of onset?
  • Recent URTI?
  • Local insect bite, impetigo or conjunctivitis?
  • Trauma?
  • Eye pain, visual acuity, headache?
  • Erythema/swelling of lid/surrounding tissue.
  • Conjunctiva – white or red/swollen.
  • Impaired eye movement (ophthalmoplegia).
  • Painful eye movements.
  • Impaired visual acuity.
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19
Q

presentation of pre-septal and orbital cellulitis

A

Pre-septal cellulitis

  • Ocular itching is a prominent symptom.
  • Bilateral conjunctival redness and swelling.
  • Symptoms on exposure.
    **Conjunctivitis **
  • Redness and discharge from one eye.
  • Affected eye ‘stuck shut’ in the morning.
  • Colour/consistency depends on cause.
  • Caused by bacteria (Staph. Aureus, H. Strep,
    H. Influenzae) chlamydia, viruses.
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20
Q

pre-septal vs orbital cellulitis

A

Pre-septal cellulitis: inflammatory disease of the orbit limited to the tissues anterior to the orbital septum.

Orbital cellulitis: inflammatory disease of the superficial and deep structures of the orbit.

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21
Q

aetiology of pre-septal cellulitis

A
  • 85%+ cases are pre-septal cellulitis.
  • Commonly follows URTI and sinusitis (ethmoid commonest).
  • Respiratory pathogens (Streptococcus, Haemophilus) commonest.
  • Other sources: spread from skin, lachrymal ducts, middle ear etc.
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22
Q

examiantion for pre-septal vs orbital (more serious) cellulitis

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23
Q

management of pre-orbital sepsis

A
  • Admit.
  • IV access.
  • FBC/CRP, cultures.
  • Nose swab.
  • IV Ceftriaxone.
  • ± IV Metronidazole
  • (if sinuses involved)
  • Prompt ENT and
    Ophthalmology
    review.
  • 4h obs.
  • Consider CT scan.
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24
Q

pneumonia differentials

A
  • Bronchiolitis (Viral CAP). * Pertussis.
  • Heart failure.
  • Sepsis.
  • Metabolic acidosis.
  • Non-infectious mimics.
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25
pneumonia differentials
* Bronchiolitis (Viral CAP). * Pertussis. * Heart failure. * Sepsis. * Metabolic acidosis. * Non-infectious mimics.
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signs of pneumonia
fine crackles bronchial breathing reduced air entry wheeze
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Fine crackles:
* Short, explosive, non-musical sounds. * Heard during mid-to-late inspiration. * Sounds like Velcro being gently separated. * Made by sudden opening of small airways. * NOT affected by coughing. * Also heard in: pulmonary fibrosis. heart failure.
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Bronchial breathing:
Bronchial breathing: * Heard in both phases of respiration. * Sounds like tracheal sounds. * Indicates airway surrounded by consolidated lung tissue – transmitting sound to surface.
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Reduced air entry. .
* Consolidation with embedded airways blocked by inflammation or secretions
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Wheeze:
* High-pitched usually expiratory sound. * Suggests airway narrowing. * Can be present in pneumonia.
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investigations severity assessment for pneumonia
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bacterial vs viral caap presentation
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management of CAP
ALL suspected bacterial CAP need antibiotics Oral for moderate CAP unless can’t tolerate. IV for severe/complicate ± moderate. Duration depends on severity and response. - Non-severe: Amoxicillin ± Clarithromycin. - Severe: Co-amoxiclav ± Clarithromycin. -or- Cefuroxime ± Metronidazole
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define Brief Resolved Unexplained Event BRUE - formerly *acute life-threatening event*
A sudden, brief, now resolved episode in an infant with: * Cyanosis or pallor, * Absent, decreased or irregular breathing, * Marked changes in tone (hypo- or hyper-tonia), * Altered level of consciousness Applies only when no other explanation after assessment 1. Brief = <1 minute. 2. Now resolved = infant asymptomatic on presentation. 3. 3. With = 1 or more criteria.
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BRUE risk screening for discharge
* Age >60 days * If premature: born at gestational age >32 weeks and current postconceptional age >45 wks. * Only 1 BRUE (NO prior BRUE i.e., first event). * Duration of BRUE <1 minute. * NO CPR required by trained medical care provider.
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low risk BRUE management
* Educate caregiver; offer CPR training. * ± ECG and O/N monitoring.
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high risk BRUE management
* Admit for continuous oximetry observation. * ECG. * FBC, bicarbonate, glucose, metabolic screen. * Blood and urine culture. * Respiratory virus testing; Pertussis testing. * Observe/evaluate feeding. * Prescribe anti-reflux medication. * Home monitoring.
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Asthamtic history
* Acuity of onset? * Potential trigger - recent URTI? allergen exposure? **Background asthma history?** * Regular asthma medication. * Frequency of preventer use. * Frequency of/last course of oral steroids. * Previous ED and GP attendances. * Social impact – days off school. **Risk of severe asthma?** * Repeated ED attendance esp. In last year. * Previous admissions, esp. in last year. * Previous near fatal asthma (ICU admission). * Pulse and respiratory rates; SpO2 in air. * Work of breathing – use of accessory muscles. * Breath sounds – unequal, silent chest? * Amount of wheeze. **Other causes/complications? ** * Pneumonia * Pneumothorax.
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assessment of asthma severity
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management of acute asthma exacerbation
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history for croup
* Acuity of onset? * Any preceding symptoms: runny nose; fever? * Other symptoms: Toxicity (very high To). Choking episode/trigger. Drooling. Voice changes/hoarseness. Cyanotic episodes. * Vaccinationstatus? * Abnormal respiratory sounds/stridor. * Respiratory status – RR; WOB.
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what is croup
common (>95%) cause of laryngotracheal infections * Typically occurs between 6mo and 6yr (peak 2yr).
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aetiology of croup
Parainfluenza virus (commonest). Influenza virus, RSV, Adenovirus. Measles.
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presentation of croup
hoarse voice. barking cough. stridor. ± fever.
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differential for croup
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stridor, stertor or wheeze
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scoring croup
Westley croup severity score
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management of croup accoridng to Westley severity
49
epiglottitis
Epiglottitis is inflammation and swelling of the epiglottis. It's often caused by an infection, but can also sometimes happen as a result of a throat injury. The epiglottis is a flap of tissue that sits beneath the tongue at the back of the throat.
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aetiology of epiglorttiis
Epiglottitis is inflammation and swelling of the epiglottis. It's often caused by an infection, but can also sometimes happen as a result of a throat injury. The epiglottis is a flap of tissue that sits beneath the tongue at the back of the throat.
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clinical presentation of epiglottitis
.
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children with epiglottiis may sit in a certain position
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management of epiglottitis
1) Secure the airway 2) Give oxygen if sats <92% 3) IV antibiotics (e.g. ceftriaxone) 4) Steroids (i.e. dexamethasone)
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sickle cell
* Autosomal recessive inheritance. * Commonly in black and Afro-Caribbean people
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natural hisotry of sickle cell disease
Common factor in distribution is history of malaria or migration from a malaria area. * Carrier offers protection against malaria.
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sickle cell disease pathophysiology
* Mutation in the Beta-globin gene. * Changes 6th amino-acid - glutamine to valine. * HbS is insoluble when deoxygenated forming * polymers which damage red cell membranes. * Results in rigid sickle shaped cells which tend * to cause vaso-occlusion; causes cascade of * pathological events: Infarction, vasculopathy, * haemolysis, inflammation.
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acute clinical manifestatins of sickle cell
anaemia acure anaemia infection painful crises priapism
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Infection in Sickle cell disease?
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longterm problems in sickle cell disease
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investigations for sickle cell
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when to admit to hospital : sickle cell
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management principles for sickle cell diagnosis
* Oxygenation. * Pain relief (within 30 minutes). * Fluid replacement (PO or IV): * Reduced tubular concentrating. * High viscosity worse sickling. * Red cell transfusion (urgent) * Broad spectrum antibiotics.
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key points about sickle cell disease
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meningitis history and examination
* Acuity of onset? * Any recent infection e.g. viral URTI/herpes? * Altered behaviour: - drowsiness/lethargy - irritability, confusion * Poor feeding/off feeds; vomiting? * Photophobia? * Seizures? * Full/bulging fontanelle (<18 months). * Neck stiffness, +ve Brudzinski/Kernig signs. * Focal neurological signs/papilloedema.
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differential diagnosis for meningitis
* Bacterialmeningitis. * Viral meningitis. * Viral encephalitis. * Tuberculous meningitis. * Cerebral abscess. * Hydrocephalus. * Non-accidental injury.
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bacterial meningitis ABCDE assessment
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management of bacterial meningitis
Sepsis 6 Lumbar puncture
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lumbar puncture contraindications
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Typical changes in the CSF in meningitis or encephalitis
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Acute management of bacterial meningitis
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complications of bacterial meningitis
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meningococcal septicaemia aetiology
VERY HIGH RISK OF MORTALITY - 12 capsular serotypes; commonest in UK (B,C, W, Y). - Carried in nasopharynx: - rate low in infants/young children. - 25% of adolescents. - 5-11% of adults. - 5-11% of adults. - Droplet spread; needs prolonged close contact. - Not understood why disease develops in some individuals.
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presentation of meningococcal septicaemia
* incubation period of 2-7 days. Prodrome: coryzal (‘flu-like’) illness. * fever. * poor feeding, vomiting, diarrhoea. headache, irritable, drowsy, seizures. * Rash present in only 80% at presentation.
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risk factors of meningococal carries becoming unwell
Age, season (Winter), smoking. Preceding Influenza A infection. Living in ‘closed’/’semi-closed’ community.
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is meningococcal meningitis the same as meningococcaemia
Meningitis can occur with/without septicaemia Septicaemia can occur with/without meningitis
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management of meningococcal septicaemia
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common causes of seziures
* Febrile convulsions * Known epilepsy ± acute illness * Meningitis or encephalitis * Hypoglycaemia/hypocalcaemia * Metabolic/Poisoning * Trauma – accidental or non-accidental
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Febrile convulsion
* 6 months to 5 years – no prev. neurology. * Generalised in nature. * Less than 15 minutes duration. * No IC infection/metabolic disturbance. * Simple or complex. * Recurrence risk 30-40%.
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Infantile spasms
* Age of onset: 3-12 months. * Sudden violent flexor spasms of head, trunk and limbs followed by extension of arms. * Last 1-2 seconds; occur multiple/day. * Often with developmental regression. * EEG: hypsarrthymia; Rx ACTH, steroids.
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Absence Epilepsy
* Age of onset: 4-12 years; girls>boys. * Sudden onset; last few seconds (<30). * Associated with automatisms – flickering of eyes, purposeless movement of eyes/mouth. * EEG: 3 per second (hz) spike and wave. * Spontaneous remission in adolescence.
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investigations for seizure
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managment of a seizure
1) ABCDE (DONT EVER FORGET GLUCOSE) 10 mins 2) Benzodiazepine - IV/ IOacces- Lorazepam - no IV access- Midazolam (buccal), diazepam (rectal) 10mins Still fitting? 3) Lorazepaman IV +- Paraldehyde PR 10 mins Still fitting? 4) **Phenytoin IV/IO Phenobarbitone IV/IO** Still fitting? 5) Rapid sequence induction (RSI) with thiopentone to ge thold of airway after 30 mins = Status epilepticus
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Status epilepticus
A seizure that lasts longer than 5 minutes, or having more than 1 seizure within a 5 minutes period, without returning to a normal level of consciousness between episodes is called status epilepticus
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differentials: 6-year-old boy presents to ED with a fever and an acute antalgic gait.
* Transient synovitis. * Septic arthritis. * Osteomyelitis. * Trauma; non-accidental injury. * Malignancy (leukaemia,neuroblastoma). * Perthes disease. * Juvenile idiopathic arthritis.
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presentation of septic arthritis
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investigations for septic arthritis
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management of septic arthritis
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Atraumatic limp summary
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clinical presentations of dehydration e.g. due to sickness and diarrhoea
90
history, examination and investigations for dehydration
* Onset, frequency (stools/vomits), duration. * Number times urinated in past 24 hours. * Risk factors for dehydration? * Other family members/contacts unwell? * Recent foreign travel? * Consumption of unsafe foods - takeaway, BBQ? * Clinical evidence of dehydration * Features suggestive of hypernatraemia
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risk factors for dehydration
* <1 year old, especially <6 months old * Low birth weight * Signs of malnutrition * Stopped breastfeeding during illness * Not offered/not tolerated fluids before presenting * >5 episodes of diarrhoea in past 24h – or – * >2 vomits in past 24h
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managment of dehydration based on severity
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presentation of DKA
**Early:** Most common – the ‘classical triad’: * Thirst (excessive drinking/polydipsia). * Polyuria. * Weight loss (over short period of time). **Less common:** * Fatigue. * Enuresis (secondary). * Polyphagia (excess hunger/eating). * Recurrent infections (e.g., candida) **Late (diabetic ketoacidosis):** * Smell of ketones. * Nausea and vomiting. * Dehydration. * Hyperventilation due to acidosis. * Abdominal pain. * Drowsiness. * Hypovolaemic shock. * Coma and death.
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criteria for diagnosiing T1DM
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Pathophysiology of Diabetic Ketoacidosis
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management of DKA
97
types of insulin
Paediatrics (Y4)
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