Acute presentations Flashcards
(97 cards)
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).
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
3
Q
screening for sepsis
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4
Q
managment of sepsis
A
5
Q
anaphylaxis
A
- Severe, life-threatening allergic reaction that is acute in onset and can cause death.
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.
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
8
Q
management of suspected anaphylaxis
A
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.
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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Q
presentation of acute urticaria
A
Presentation
- Intensely pruritic rash
- Agitated, irritable, unhappy
- Spreading rash
- Raised erythematous plaques
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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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Q
paracetamol overdose protocol overview 1/2
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14
Q
history for paracetamol overdose
A
o Dose
o Timing
o Associated ingestions
15
Q
paracetamol overdose protocol overview 2/2
A
16
Q
management of paractermaol overdose
A
charcoal only if very recently ingested
defintive treatment: N-acetylcysteine infusion
17
Q
differential diagnosis
A
* Pre-septal cellulitis.
* Orbital or Post-septal cellulitis. * Allergicconjunctivitis.
* Bacterial conjunctivitis.
* Trauma.
* Sub-periostal/orbital abscess. * Cavernous sinus thrombosis.
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.
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.
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.
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.
22
Q
examiantion for pre-septal vs orbital (more serious) cellulitis
A
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.
24
Q
pneumonia differentials
A
- Bronchiolitis (Viral CAP). * Pertussis.
- Heart failure.
- Sepsis.
- Metabolic acidosis.
- Non-infectious mimics.
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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
40
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.
42
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
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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
67
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
82
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
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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
96
management of DKA
97
types of insulin
