The limping or non-weight bearing child is a common general practice and emergency department presentation, that can cause a lot of stress for parents.

There are also a wide range of differentials, although most of these can easily be narrowed down by age. Thankfully, most of the differentials are not emergencies, but there are some serious things not to be missed.

The majority of cases will likely be transient synovitis (or no cause identified). This is a benign disorder

Differentials

• Non-accidental injury – NAI
• Developmental dysplasia of the hip – DDH
• Transient synovitis
• Perthes disease
• Slipped capital femoral epiphysis (SCFE)
• Septic arthritis
• Viral myositis
• Toddler’s fracture
• Reactive arthritis or other rheumatological disorder

History

• Duration of symptoms
• Speed of onset
• Limp or complete refusal to weight bear?
• History of trauma?
  • There may often be a history of (typically mild) trauma that is incidental
• Preceding illness?
  • Recent viral infection? (Transient synovitis or reactive arthritis)
• Any fever?
• Location of pain
  • Often difficult to localise, especially in children <5 years
• Morning stiffness? (Rheumatological disorder)
• Any previous injuries or other child protection concerns?

Examination

• General appearance
• Temperature
• Gait
• Neurological examination
  • Weakness
• Bruising
  • Excessive or not in keeping with accidental injury
• Abdomen
  • Check for tenderness, including inguinal area (masses)
  • In boys – if any abdominal pr inguinal pain – check the scrotum!
• Lower limb
  • Bony tenderness
  • Assess hip, knee and ankle
    • Hip pathology suggested by restricted internal rotation and abduction
  • Check lumbar spine and sacrum

Investigation

• If limp <3 days duration, no history of trauma and afebrile, investigation is not typically required
• If septic arthritis suspected (fever, often severely restricted movement), then consider:
  • FBC
  • CRP / ESR
  • Blood cultures
  • USS – can show effusion in septic arthritis of hip joint
• If limp >3 days duration, or history of trauma, consider imaging:
  • X-ray, typically of hip and knee, “frog leg lateral view” is good for spotting SCFE
  • Bone scan can spot areas of increased bone turnover, and as such may help to identify:
    • Osteomyelitis
    • Discitis
    • Perthe’s disease
    • Occult fracture

Management

• Depends on the underlying disorder
• See individual topic articles

In the case of transient synovitis, or no cause identified:

In my experience, many non-specific cases in otherwise well toddlers improve dramatically with NSAIDs and a short wait (an hour or so) and can be safely discharged from the Emergency Department or GP surgery. In cases with a fever, give NSAIDs whilst the results of FBC and CRP are awaited, and if normal this is typically enough to exclude septic arthritis if the child’s walking improves, and I would discharge these patients home with NSAIDs and close FU (e.g. advise review with the GP the following day). The cases of septic arthritis I have seen tend to be pretty obvious – with a clearly distressed child refusing to move the limb at all, but be wary that early septic arthritis may not be so severe – Dr Tom Leach

Summary of disorders

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy
• Child with limp – RCH

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Serotonin syndrome is an iatrogenic (caused by medical intervention) syndrome, that results from excess serotonin levels in the central and peripheral nervous system, typically as the result of the use of one or more drugs known to cause an increase in serotonin levels.

For serotonin syndrome to be diagnosed, symptoms must coincide with the introduction of a serotonergic medication.

Rare, it can occur with a single medication, but most commonly it occurs when a new medication is added to a patients medication list, at a time when they are already taking at least one other serotonergic medication. It can also occurs if a patient changes between anti-depressants without an effective “washout period”.

• It may also be seen in cases of accidental drug ingestion in children

It is a relatively rare disorder.

In my experience, the most common combination is the use of Tramadol with SSRIs. In fact, this is the only circumstance in which I have seen serotonin syndrome. – Dr Tom Leach

The main treatment is cessation of the offending drugs – cease all serotonergic drugs.Most cases are mild and self limiting. In severe cases, patients may need ICU admission, and it can be fatal, although this is rare. If serotonin syndrome is suspected in the community – refer immediately to the emergency department.

Occasionally sertonergic antagonists such as cyproheptadine may be used.

Medications known to cause serotonin syndrome

• SSRIs
• SNRIs
• MAOIs
• Tricyclic antidepressants
• Tramadol
  • A synthetic opiate with serotonergic effects. The exact mechanism seems a little unclear, although some sources report that one if its metabolites is an SSRI
• Tapentadol
  • Similar to tramadol
• Other opioids
  • Rare
• St Johns Wort
• Stimulants
  • Particularly MDMA (“ecstasy”)
  • LSD
  • Amphetamines
  • Cocaine

Presentation

The diagnosis is clinical, based on a combination of the signs and symptoms below, in conjunction with a history of use of serotonerigc drugs – particularly in combination, and particularly if one or more were started within the last 2 weeks.

• Psychiatric effects
  • Agitation
  • Confusion
  • Hypomania
  • Seizures
• Muscle / peripheral neurological effects
  • Increased muscle tone
  • Tremor
  • Shaking
  • Hyperreflexia
  • Clonus
  • Hyperreflexia and clonus are particularly important and often specific signs
• Autonomic effects
  • Hypertension or hypotension
  • Tachycardia
  • Fever
  • Diarrhoea

An example of clonus in the lower limb of a patient with serotonin syndrome. Almostadoctor original content.

Investigations

Investigations are not required for the diagnosis, but may help to rule out other suspected conditions. In serotonin syndrome, there may be:

• Increased WCC
• Increased CK

Management

Cease the offending drugs!

Mild cases

• Most will resolve within 72 of the cessation of the offending drugs
• Hospital admission may not be required

Severe cases

• May require ICU admission. The main indication for this is hyperthermia
• Potential complications include
  • Hyperthermia
    • Should be treated aggressively – e.g. with ice packs, cooling sprays. Occasionally requires paralysation and intubation with ventilation
  • Rhabdomyolysis
  • ARDS
  • DIC – disseminated intravascular coagulation
  • Hypertension
    • Specific treatment is often not required
  • Seizures
    • Typically treated with benzodiazepines
  • Renal failure
• Cyproheptadine
  • May be used for its serotonin-anatagonistic effects
  • Typically given orally as 4-8mg dose
  • Repeat in 2 hours
  • If effective, give 8mg QID

References

• Serotonin Syndrome – NPS Medicinewise
• Serotonin Syndrome – RCH
• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

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• Superficial aka first degree – epidermis (erythema) only. Can be differentiated from partial thickness by rubbing the skin. If the epidermis moves around, sliding over the deeper layers, this is a partial thickness burn
• Partial thickness aka second degree – affects the dermal layers. Can be sub-divided into superficial dermal, mid dermal, and deep dermal
• Full thickness aka third-degree – all the way through the dermis and may also affect deeper tissues

Calculating burns area

• Only include partial and full thickness areas
• Remember that a single burn likely has patches of different thicknesses
• If unsure if superficial or partial thickness, be cautious and include affected areas
• Rule of 9’s
• Useful because it allows for estimation of Total Body Surface Area of burn, which is later used in the calculation for fluid requirements

Fluid Requirements

• Burns leads to lots of skin oedema which can cause hypovolemic shock
• The modified parkland formulais used to calculate fluid requirements
• Should be given if TBSA burns >15% in adults and >10% in children
• Don’t forget other factors that may lower your threshold for giving fluids, including other traumatic injuries, or inhalational burns
• Hartmann’s is fluid of choice
• First ½ of the fluid should be given in the first 8 hours after the burn (not after the presentation)
• Second half over the next 16 hours
• Formula:
  • 4mls x TBSA Burn % x Weight (Kg)

Important Factors in History

• Time burns occurred
• Duration of exposure (helps assess burn depth)
• Enclosed area? (Inhalation injury)

First Aid

• Try to remove jewellery and clothing as appropriate. If clothing is stuck to burn, leave it alone
• Choice of dressing varies widely between centres. Check local policies
• Running under cool water can help. You should od this for 20 minutes or so, and is only useful if <3hours since burn. Be aware that if there is a large burn surface area, this can cause hypothermia

Specialist Management

• Any patient with >10% TBSA (>5% in children) burns should be considered for transfer to burns unit. If there is any doubt about this, speak to the local burns centre for advice.
• Other potential factors that might lower the threshold for transfer include:
  • Very young
  • Very old
  • Pregnant
  • Other significant co-morbidities or trauma
  • Chemical burns
  • Circumferential burns

Inhalational Injury

• Occur in 20% of burns patients
• 60% of facial burns patients
• major cause of mortality

Causes of pathology in inhalational injury

• Thermal injury to the airway
• Chemical injury to the airway
• Systemic effects from toxins (CO, cyanide – as a combustion product of some plastics / wools etc)
• Hypoxia / asphyxia due to O2 consumption by the fire

Signs of airway injury

• Upper airway
  • Singed nostrils / nostril hairs
  • Singed eyebrows
  • Facial burns
  • Soot in nose
  • Change in voice / hoarseness
  • Stridor
• Lower airway
  • Wheeze
  • SOB
  • Pulmonary Oedema

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This is colloquially known as a ‘head rush’ or ‘dizzy spell’, and is unsteadiness or LOC on standing from lying in those with inadequate vasomotor reflexes. It is defined as a fall in systolic BP of 20mmHg+ or a fall of diastolic BP by 10mmHg+ when an individual assumes a standing position.

Those at risk include:

• The elderly
• Those with autonomic neuropathy
• Those on antihypertensive medications
• Overdiuresis
• Multi-system atrophy (MSA)

Postural hypotension is an important cause of falls and faints in the elderly.

Physiology

• The symptom of orthostatic hypotension results from the gravity-induced pooling of blood in the lower extremities following a change in posture.
• This pooling of blood compromises venous return, thus lowering cardiac output and subsequent arterial pressure.
• This ultimately leads to insufficient perfusion of the upper body with blood.
• In health, the blood pressure does not fall very much upon standing because the baroreceptor reflexis triggered.
• This process is mediated by the autonomic nervous system. Carotid sinus baroreceptors are innervated by CN IX and the aortic arch baroreceptors are innervated by CN X.
• Baroreceptors are stretch-sensitive mechanoreceptors. High blood pressure causes distension of blood vessel walls, which stimulates the baroreceptors to fire action potentials at a faster rate. This leads to inhibition of the sympathetic nervous system and activation of the parasympathetic nervous system.
• In contrast, when blood pressure falls, blood vessel walls are less distended; this is recognised by the baroreceptors which stimulate sympathetic activation and parasympathetic inhibition, thereby triggering vasoconstriction and an increase in heart rate in order to elevate the blood pressure, press blood up into the body again, and avoid the ‘dizzy spells’ we have mentioned.
• Secondary factors which cause a greater than normal fall in blood pressure are often responsible for orthostatic hypotension; factors such as hypovolaemia, sepsis, systemic vasodilatation or diuretics mean that the sudden change in blood pressure cannot be compensated for by the reflex.
• Avoiding orthostatic hypotension relies on being able to maintain an adequate blood supply, which relies upon a heart strong enough to pump, arteries and veins which are able to constrict when necessary, and having enough blood and fluid within the vessels. Interruption in any of these can thus lead to problems.

Aetiology

• Hypovolaemia:
  • Dehydration (vomiting, diarrhoea, fever, heat stroke)
  • Blood loss
  • Excessive use of diuretics
  • Vasodilators
  • Prolonged bed rest
  • Anaemia
• Disease:
  • Addison’s disease
  • Atherosclerosis
  • Autonomic neuropathy
  • Diabetes (peripheral neuropathy may affect the autonomic nervous system and thereby interfere with the baroreceptor reflex)
  • Phaeochromocytoma
  • Parkinson’s disease
  • Heart disease
  • Hypopituitarism (low ACTH)
• Medication:
  • Beta blockers (block the beta-adrenergic receptors in the body and prevent the heart rate from increasing, the heart from contracting as forcefully as is possible, and the dilatation of blood vessels)
  • Sildenafil (Viagra – works by dilating blood vessels and its effects are magnified if taken in conjunction with nitrites, so beware in patients with Angina!)
  • Tricyclic antidepressants
  • Monoamine oxidase inhibitors

Clinical Features

Upon moving from a sitting or lying to a standing position:

• Lightheadedness
• Weakness
• Blurred vision
• Syncope/LOC
• Distortion in hearing
• Seizures

These are the consequences of inadequate cerebral perfusion as a result of the blood pressure being too low. This may lead to a vasovagal episode to be stimulated, otherwise known as vasovagal/ neurocardiogenic syncope.

Vasovagal Syncope

• Emotion, pain, fear, or standing for too long can stimulate reflex bradycardia +/- peripheral vasodilatation.
• Excess activation of the parasympathetic system causes the heart rate to slow and blood vessels to dilate.
• Onset is over seconds, and is preceded by nausea, pallor, sweating and closing in of visual fields (a phenomenon known as ‘pre-syncope’).
• Patients may lose consciousness for ~2mins. This, as well as symptoms of dizziness occur due to the lowering of blood pressure and decrease of blood flow to the brain.
• The vagus nerve that causes this response may also in some cases be triggered by micturition (especially in men) or by severe straining with constipation.
• Brief clonic jerking of the limbs may occur (reflex anoxic convulsion due to cerebral hypoperfusion) but there is no stiffening or tonic àclonic sequence, and it can thereby be distinguished from a typical epileptic seizure of that nature.
• Post-ictal recovery is rapid.

Diagnosis of Orthostatic Hypotension

• Ensure patient has been lying down for at least 5 mins and is relaxed
• Explain procedure and obtain consent
• Take sitting or lying blood pressure with the arm supported at heart level, e.g. on a pillow
• Leave the cuff in place and ask patient to stand
• Allow the patient to stand for three minutes
• Ensure their arm is once more supported at heart level and repeat blood pressure
• Record results

Diagnose orthostatic hypotension if there is a drop in systolic BP of >20mmHg or a drop in diastolic BP of >10mmHg after standing for 3 minutes vs lying down.

Management

Conservative:

• Lie down if feeling faint
• Stand slowly (with escape route, e.g. a chair to fall back on)
• Consider referral to a ‘falls clinic’
• Manage any autonomic neuropathy
• Increased water and salt ingestion can help
• Physical measures such as leg crossing, squatting, elastic abdominal binders/stockings (must check dorsalis pedis pulse is present) and careful exercise may help
• If prost-prandial dizziness, eat little and often and reduce carbohydrate and alcohol intake
• Head-up tilt of the bed at night increases renin release, so decreases fluid loss and increases standing blood pressure

Medical:

• Fludrocortisone (retians fluid). Monitor weight and beware if CCF or low albumin: oedema worsens.
• Sympathomimetics e.g. midodrine or ephedrine. Can give pyridostigmine if detrusor under-activity too.

References

Read more about our sources

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The vomiting child is a very common presentation to general practice and emergency departments. By far the most common cause is an infective (usually viral) gastroenteritis, but it is very important to bear in mind the broad range of differential diagnoses, and remember that vomiting in children is a sign of many serious illnesses, as well as a common indicator of gastroenteritis.

Important causes to consider include:

• Surgical – e.g. obstruction, intussusception, appendicitis. Ask about pain, distention, bile in vomitus
• Infection – ?UTI, ?Meningitis. Suspect if high fevers
• Metabolic Conditions – Diabetes, Haemolytic Uraemic Syndrome. Suspect if Polydipsia, polyuria
• Injury – in particular head injury with vomiting – raised ICP / headache

Typically:

• Vomiting AND diarrhoea, is more likely to be gastroenteritis
• Vomiting WITHOUT diarrhoea is more likely to be indicative or a more serious underlying cause, especially with fever and / or pain

Dehydration

Think about fluids in vs fluid out. It is difficult for parents to accurately assess intake. The easiest way to assess this is with the proportion of their norma intake.

• Ask about proportions
• <50% of normal fluid intake
• Wet nappies – >8hrs between wet nappies is a warning sign / at least 3 wet nappies per day is the bare minimum of normal
• Abnormal losses – >5 episodes of D or V

Degree of dehydration

• MILD <5%
  • Thirsty
  • Reduced urine output
  • Dry mucosa
  • Mild tachycardia
  • TREATMENT – smaller, more frequent feeds (breast / formula / or oral rehydration fluids). If unsuccessful – to ED for rehydration. NG or IV.
• MODERATE 5-10%
  • As above, plus
  • Lethargy
  • Sunken fontanelle / eyes
  • Reduced skin turgor
• SEVERE >10%
  • As above, plus
  • Decrease in level of consciousness
  • Signs of shock (hypotension, poor perfusion, cap refil etc)

Treatment

• Children with signs of shock need urgent rehydration with IV fluids
• Otherwise – oral rehydration is usually the preferred method
• If breast-fed and young (<1 year) then more frequent breast feeds are the preferred method
• If this is not tolerated, or an older child, then oral rehydration fluids are preferred option. However, these are often not well tolerated. One study has shown that apple juice was as good if not better than oral rehydration fluids – probably because children prefer the taste and so drink more of it! In younger children, diluting the juice may be preferable (e.g. ½ or ¼ strength).
• Children (and parents) may need a lot of encouragement. Most emergency departments will have a protocol with an oral rehydration chart – and parents will be encouraged to give a set amounts – e.g. 10mls every 10 minutes – via an oral syringe if the child is really struggling

BEWARE

• Dystonic reactions. Stemetil and metoclopramide are CONTRAINDICATED IN CHILDREN. Most common in children under 2 years. Benztropine is a good anti-dystonic, but can only be used in children over 1 yr. In children <1yr, antihistamines / diazepam should be used
  • Dystonic reactions are most common in children under 2 and rare in children over 11
  • Can be treated with benztropine in children over 1
  • In children under 1 – consider diazepam
• Ondansetron is suitable, even in mild dehydration – doses recommended by the Royal Children’s Hospital in Melbourne are:
  • Weight 0-8Kgs – DO NOT USE
  • Weight 8-15kgs – 2mg Ondansetron TDS PRN
  • Weight 15-30kgs – 4mg Ondansetron TDS PRN
  • Weight 30+Kgs – 8mg Ondansetron TDS PRN
• If rehydration still fails – consider NG tube rehydration of IV fluids

Sources

• RCH – Gastroenteritis

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Definition: Febrile neutropenia is the presence of a fever > 38^oC and with an absolute neutrophil count of <1.0×10⁹/L ^[1]
Note that in many hospital policies, patients may be considered to have febrile neutropenia if they have a recorded fever and recent (usually within last 2 weeks) chemotherapy, even if the neutrophil count is not (yet) low.

• Neutropenia occurs due to bone marrow suppression
• Patients with neutropenia are less likely to produce an effective immune response to infection
• Bone marrow suppression is common side effect of chemotherapy, but has many other causes (anaemias, genetic defects drugs, infections)
• Patients are at a very high risk of developing life threatening bacterial infections and sepsis
• Infection should always be considered in patients who are systemically unwell, and who are receiving chemotherapy, even though fever may not be present.

Key Points

• Suspect febrile neutropenia in all patients receiving chemotherapy who develop a fever ( >38^oC) or patients appear systemically unwell
• ALWAYS ask patients who have recently been diagnosed with cancer if they are receiving chemotherapy, as this information may not always be offered
• In all suspected FN cases, patients should be referred to the hospital (preferably the oncology team) for an urgent FBC, assessment and consideration of immediate antibiotic therapy.
• If FN suspected, DO NOT wait for FBC results, as patient may deteriorate rapidly
• National guidelines state that all patients should receive (IV broad spectrum) antibiotics within 60 minutes. ^[2]

Signs and Symptoms

Symptoms can be non-specific and can have no localised features.

• Feeling hot/cold
• Rigors
• Sweats
• Flu like symptoms
• General malaise
• Ask about sore mouth or diarrhoea as this is common as chemotherapy
• Mucositis can be an entry route for host flora into the blood stream

Initial Clinical assessment

History

• Patient in high risk group?
• Renal failure
• When was last chemotherapy cycle?
• Any recent blood products
• Any Intravascular devices
• Check past microbiology results for any history of resistant organism

Examinations

• Cardiac and respiratory symptoms
• Pyrexia,  stigmata of infective endocarditis, skin rashes, lymphadenopathy
• Potential foci of infection
• ENT examination
• Fundoscopy
• GI tract
• Respiratory system
• Genitourinary tract
• Neurological (e.g. signs of meningism)

Investigations

• FBC (check the neutrophil level!)
• Two blood set cultures from a peripheral vein, and any indwelling venous catheters
• Radiological investigations also can be performed if needed
• Other Investigations
• Blood film , D-dimer and fibrinogen testing
• U+E, creatinine
• LFT
• CRP, ESR
• CXR
• Coagulation screen
• Serology/polymerase chain reaction for virus (e.g. CMV)
• Other specialised investigations include: bronchoscopy and CT scans

Management of febrile neutropenia

• Empiric IV broad spectrum antibiotic therapy, according to the local policy. Should be done before FBC results if patient in shock
• Supportive measures: IV fluids, if necessary
• Colony stimulating factors may be considered in high risk patients, with prolonged (>10 days) or serious neutropenia (<0.1×109/L), hypotension and multi-organ failure

• Oral antibiotics: Only in some low risk FN patients. Haemodynamically stable and also who DO NOT have: pneumonia, acute leukaemia, evidence of organ failure, indwelling venous catheter and severe soft tissue infection

• Quinolone with amoxicillin + Clavulanic acid is the most preferable choice, due to the rise of Gram+ FN episodes.
• Oral quinolone should be avoided in patients who have quinolone antibacterial as prophylaxis
• NICE suggest that all patients requiring IV treatment should be started on a β-lactam monotherapy, with piperacillin and tazobactam
• Aminoglycosides should be AVOIDED for initial empirical therapy, unless specific patient or local related reasons

• Coverage of MRSA or gram negative bacteria may be required. Pneumonia diagnosed, antibiotic cover extended for treatment of atypical organisms. Adding a macrolide antibiotic.

Multinational Association for Supportive Care in Cancer (MASCC) index can be used as a risk assessment tool to assess whether a patient is low or high risk.

References

[1] Naik, JD et al. (2011). Febrile neutropenia. British Medical Journal. 342 (1), 103-104.

[2] Rull,G et al. (2012). Neutropenic Patients and Neutropenic Regimes. Available: http://patient.info/doctor/neutropenic-patients-and-neutropenic-regimes. Last accessed 29/01/2016.

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Cardiac Tamponade is a condition where the heart become compressed by excess fluid in the pericardium. Compression causes reduced diastolic filling of the heart, which can cause cardiac arrest.

The pericardiac sac is normally a virtual space. This is enclosed by the pericardium.

Causes of Cardiac Tamponade

• Traumatic injury – particularly penetrating injury – can lead to accumulation of blood in the pericardial sac. This compresses the heart, and prevents diastolic filling, which leads to cardiac arrest. Cardiac Tamponade in a trauma setting an emergency and can quickly become life-threatening.
• Pericarditis
• Cancer
• Iatrogenic – can occur after cardiothoracic surgery

Presentation

• Becks Triad – occurs in about 1/3 of patients with cardiac tamponade
  • Hypotension
  • Distended Neck Veins
  • Muffled Heart Sounds
• Tachycardia
• Shortness of breath
• Chest pain
• Pulsus Paradoxus – systolic BP decreases >10mmHg on inspiration
• Have a high index of suspicion in any patient with penetrating chest injury – especially they are not responsive to IV fluids and other basic investigations
• FAST / bedside echo can diagnose without the need for other imaging (which may be time consuming)
• It quickly causes cardiac arrest!

Management

• Pericardiocentesis can be performed in the emergency setting in the peri-arrest scenario
  • Use a long 14 or 16G cannula attached a syringe
  • Insert at the angle of the xiphisternum and the left rib border – and aim for the ipsilateral (same side) scapula. Aspirate as you slowly advance. In reality this would often be performed US guided in the emergency department
  • Pericardiocentesis is sometimes attempted for suspected cardiac tamponade in the pre-hospital setting – but is rarely successful
• Surgery may be indicated in some patients – this may be the formation of a pericardial window or could involve a pericardiectomy
• Conservative management – may be attempted in some patients – albeit under very close monitoring (e.g. in the intensive care setting in a trauma patient)
• Involving the cardiothoracics team (and trauma team if indicated) early in management and decision making is imperative

References

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Pulse Oximetry is a way of measuring the oxygen level in the blood.

It is a measure of oxygenation but not a measure of ventilation

• Oxygenation – the ability f the body (particularly lungs) to maintain high oxygen concentration in the blood
• Ventilation – the ability of the lungs to adequately provide oxygenation and remove carbon dioxide from the blood

Therefore, pulse oximetry provides no indication of the carbon dioxide levels, or of the adequacy of ventilation. To get a better estimation of this, an arterial blood gas is required.

Normal Pulse Oximetry Values

• A normal healthy individual usually has a value in the high 90s%
• Textbook definition of normal is >93%
• ‘Normal’ for an individual with COPD or other chronic lung disease can be 88-92%

Estimating pO2 from oxygen saturations

Looking at the curve below, you can see how the curve starts to dive sharply downwards below 90%. This is why the ‘normal’ saturation cut-off is so important.

How it Works

Pulse oximetry measures the ratio of red to infrared light absorbed by the tissues. This ratio changes because the colour of haemoglobin changes depending on how saturated with oxygen it is.

The method was developed in the 1980s. Prior to this, the only way to assess oxygen saturation was with an arterial blood gas sample.

Limitations

• Depends on the adequacy of peripheral circulation. If the peripheries are cool – for example if the patent is shut down because they are very sick, then a peripheral pulse oximeter will not give a reliable reading. This problem can be alleviated by using a more centrally placed oximeter – such as a sticker on the forehead.
• Not reliable in carbon monoxide poisoning. Carbon Monoxide strongly binds to haemoglobin and can give a falsely elevated oxygen saturation. To properly assess oxygenation in CO poisoning, an arterial blood gas is required, which can give the carboxyhemoglobin concentration.
• Not reliable at very low saturations – below 70% the readings are not clinically reliable.

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Trauma is managed by teams in the Emergency Department. There is often a defined set of individuals on a ‘Trauma Team’. This might include:

• Team Leader – often an Emergency Physician / Registrar
• Anaesthetist
• Anaesthetic assistant
• Trauma (General) Surgeon / Registrar
• Orthopaedic Surgeon / Registrar
• Additional Emergency Doctors
• Radiographer
• Scribe
• Several Nursing Staff

Allocating Roles

Before the patient arrives then the roles of the team will usually be allocated. Often a ‘Trauma Code’ is sent out to the pagers of the members of the team with pre-defined roles once the message comes in from the ambulance that a trauma patient is expected.

Team leader, scribe, and other roles such as managing airway, circulation, taking blood will be discussed and allocated usually before the arrival of the patient.

Deaths in Trauma

Death in trauma can be divided into:

• Immediate – caused by major disruption or large blood vessels or body cavities
• Early – can occur in minutes to hours after the trauma. Caused by failure of oxygenation of the vital organs – often secondary to cardiovascular collapse.
• Late – occurs days to weeks after the injury. Often due to sepsis and multi-organ failure.

Training of critical care staff – such as with the ATLS (Advanced Trauma Life Support) and EMST (Early Management of Severe Trauma) protocols is aimed at reduced the number of deaths of the ‘late’ category.

The aims of the critical care team in severe trauma are to:

• Stabilise the trauma patient
• Identify life-threatening injuries
• Initiate organ saving interventions

Management of Trauma

Care in the emergency department usually begins with handover from the transporting team (usually ambulance crew). When taking this handover, you should think about the MIST pnemonic

• M – Mechanism
• I – Injury
• S – Symptoms
• T – Treatment

Primary Survey

This is based on the ABCDE approach – with an extra emphasis on the c-spine at the start of the survey. It is a very rapid assessment conducted as soon as the patient arrives in the Emergency Department designed to catch any immediately life-threatening injuries. The patient should be lying flat on their back in bed.

• C-Spine – is it immobilised? Does it need to be immobilised? Are there injuries that may have caused c-spine damage? If there is any doubt – assume c-spine injury
• A – Airway – can air pass in and out of the lungs? Is the patient conscious and breathing for themselves? Are there any visible obstructions (foreign body, vomit, secretions, patient’s tongue). Initiate airway management techniques as required – this might be anything from simple airway manoeuvres like chin lift (beware of head tilt in c-spine injury), to intubation or even performing a surgical airway!
• B – Breathing – the ability to ventilate. Is the patient breathing? Auscultate the chest. Check for chest rising and equal air entry. Look for gross chest wall defects or injuries. Check the trachea for any deviation. Be wary for pneumothorax or haemothorax – patients might need a chest drain. Flail chest segments often require mechanical ventilation.
• C – Circulation – check the BP and get an ECG if indicated. Make sure blood is sent, including FBC, Urea and Electrolytes, a blood gas, group and save and clotting. Check for signs of hypotension. Look for any signs of external bleeding. Check the heart sounds – think about cardiac tamponade. Check the abdomen for sources of bleeding, including palpating the abdomen for intra-abdominal bleeding. Try to get two large bore IV lines (if someone hasn’t done this already). Control any external bleeding with direct pressure until surgery. Consider a FAST scan to look for sources of intra-abdominal blood. Try to get two large bore cannulas into two large veins as soon as possible. 
• D – Disability – Check gross mental status. Do GCS. Check pupils. Quickly check for peripheral neurological signs
• E – Expose the patient – completely remove clothes and check for any injuries. Consider a log-roll to be able to check for spinal tenderness and rule out injuries on the back, the back of the head and the neck. You should also briefly check peri-anal sensation and anal tone. Once you have finished, make sure to put some blankets (or warmer) on the patient to avoid hypothermia.

Usually, whilst all this is going on, members of the team will be taking blood test, attaching leads for ECG, and getting IV access.

Don’t forget to repeat your survey frequently to keep on top of any changes in the patient’s condition.

Secondary Survey

This will vary a great deal depending on the condition of the patient – are they conscious and able to give a history? Is there a collateral history available?

You could base your history around the AMPLE acronym:

A – Allergies

M – Medications

P – Past History

L – Last meal – important for anaesthetic risk!

E – Event – how did it occur?

The physical examination is a full ‘top to toe’ examination

• Head – fully examine the soul and head for any evidence of injury. Examine the cranial nerves. Check the ears (haemotympanum for evidence of basal skull fracture) and nose for evidence of bleeding.
• C- Spine – check the c-spine for tenderness. Remove the collar for this, but make sure that the head is stabilised (usually by another member of staff) whilst you check the spine. Maintain full spinal precautions until the c-spine has been cleared. 
• Chest – palpate the chest wall checking for instability, rib fractures, areas of flail chest, evidence of subcutaneous emphysema. Listen again to the heart and lungs. Don’t forget to check the axilla and the back – especially in patients with any penetrating chest wounds. If any chest tubes have been places – make sure they are in place correctly and are having output. Make sure a CXR has been ordered +/- performed.
• Abdomen / Pelvis – palpate the abdomen. Check for tenderness or distension. If there is any suspicion of pelvic injury – apply a pelvic binder. Don’t forget to examine the genitals and anus for evidence of bleeding or other trauma.
• Limbs -check all 4 limbs for deformity or other evidence of injury. Split and/or reduce long bone fractures. Check for peripheral pulses. 
• Don’t forget to check the spine if it wasn’t; already done on in the primary survey
• Neurological examination – depending on the conscious level and injuries of the patient you should attempt to perform a neurological examination of the limbs
• Don’t forget to cover the patient up again at the end!

Your hospital may have a trauma pro forma that is filled in as part of the secondary survey (often with lots of diagrams and pictures to help injuries be described).

Fluids in Trauma

Be wary of giving large amounts of fluids – this can inadvertently increase the blood pressure and increase blood losses.

• Maintain a MAP (mean arterial pressure) of >65mmHg
• Aim for adequate BP – not normal BP
• Head injury patients should maintain a SBP (systolic blood pressure) of >90mmHg
• Be particularly cautious if there is internal bleeding
• Give small fluid boluses regularly as required – usually boluses of around 200mls. Avoid large amounts of fluid stat (if possible) – if parameters are maintained as above.
• If larger boluses are needed if BP drops – boluses of 10ml/Kg maximum are recommended

Haemorrhage

Defining haemorrhage is difficult. The American College of Surgeons Classification of Haemorrhagic Shock classifies haemorrhage shock in classes I – IV – with IV being the most severe.

• Blood pressure changes are late
• Pulse pressure changes are earlier
• Respiratory rate is an early change
• Mental state is an early change
• DON’T AIM FOR A ‘NORMAL’ BP
  • Aim for MAP >65mmHg
• Send a group and save and crossmatch request ASAP
  • O negative blood can be given immediately
  • Group specific blood takes about 10 minutes to be processed by the lab
  • Crossmatched blood takes about an hour to be process by the lab
• Give O negative blood as soon as possible if required
• Give blood products in the ratio of 1:1:1
  • 1 unit of RBCs
  • 1 unit of FFP (fresh frozen plasma)
  • 1 unit of platelets
• If there are signs of external bleeding – keep pressure on and don’t stop!

FAST Scan

This stands for Focused assessment Sonography in Trauma. The fast scan is an US scan performed at the bedside, usually by an Emergency Registrar or Consultant, or occasionally the Trauma Registrar or Consultant (Gen Surgery).

The scan is usually performed after the secondary survey.

The goals of the FAST scan are to find any intra-abdominal free fluid (which in this circumstance is most likely to be cause by bleeding), to check for cardiac tamponade, and to assess the lungs.

• Visualises three spaces: intra-abdominal, intra-thoracic and pericardial
• Can usually only detect blood if >200mls present
• Good pelvic views by a skilled sonographer in an easily viasulised (usually skinny person) abdomen can detect smaller amounts
• 7 Views in total
  • Subxiphoid 4 chamber (cardiac)
  • Transthoracic long axis
  • Abdominal and lower thoracic
  • Right coronal and intercostal oblique
  • Left coronal and intercostal oblique
  • Pelvic
  • Anterior thoracic

Other Imaging

• Chest XR
• Pelvic XR
• C-spine X-ray

These three scans are usually standard in most trauma patients. Other imaging should be requested based on clinical findings.

A “Pan Scan” is usually a CT scan from the Head to the Pelvis in cases of severe trauma with multiple indicated injuries.

Head Injury in Trauma

The use of fluids in head injury in trauma is a special case. In the absence of head injury – fluids should only be given if the MAP is <65mmHg.

In head injury, we give fluids to maintain a SBP of >90mmHg.

This is to prevent secondary brain injury. 

• Primary brain injury – occurs at the time of the trauma – nothing can be done to reverse this!
• Secondary brain injury – occurs in the hours after the injury and can be prevented by following the ABCDE principles
  • Often caused by hypoxia and hypotension
  • ALWAYS give oxygen and maintain SBP >90mmHg

Prognositc Indicators in Head Injury

• High energy trauma – e.g. fall from height, high speed MVA
• Low level of consciousness at presentation
• Anticoagulation
• Diffuse brain injury on CT
• Hypotension
• Age – worse prognosis in older patients

Disposition of the Trauma Patient

Obviously depends on many factors! Severe trauma will often go straight to theatre and then onto ICU.

Patients with mild trauma, especially those with head injury, will usually be admitted to the trauma ward for observation, and the following day a Tertiary Survey is usually performed.

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• Tonic Clonic Seizure lasting > 5 minutes, OR
• Two or more seizures without full recovery (GCS = 15) in between (over any time period, usually within an hour or so)

Seizures in status epileptics are almost always tonic clonic. Status epilepticus is a medical emergency

Risks

Neurological

• Primary brain injury – excitotoxic neuronal injury
• Secondary brain injury – e.g. from hyptension, hypoperfusion, hypoxia
• Excessive intracellular calcium leading to cell toxicity and death

Respiratory

• Hypoxia
• Aspiration pneumonitis
• Respiratory acidosis
• Aspiration pneumonitis

Cardiovascular

• Arrythmias
• Tachycardia
• Hypotension / Hypertension

Other

• Lactic acidosis
• Rhabdomyolysis
• Hyperglycaemia
• Hypoglycaemia

Management

Benzodiazepines are the first line management. Lorazepam IV is considered to be the best option. It has a quick onset and lasts several hours. In some studies it has also been shown to have superior seizure terminationg effects and reduced risk of sedation over diazepam. Out of hospital, or where IV access is not available, buccal or nasal midazolam is first line. Rectal diazepam is also used, but has slower onset, and its anti-seizure effects only last 20-30 minutes.

Specifics

• Lorazepam 0.1 mg/Kg IV
• IV midazolam (0.1-0.3mg/Kg), clonazepam (0.5-1mg/Kg) and diazepam (0.15mg.Kg) are all useful alternatives in the above is not available
• No IV access: Midazolam 0.15-0.3mg/Kg IM or buccal or nasal, OR rectal diazepam 0.5mg/Kg (slowest onset)
• In addition: consider phenytoin (15-20mg/Kg IV) if not ceasing
• Phenobarbitone should be added as the second line agent if the above are still not effective. Patient must be ECG monitored.Dose of 10-20mg/Kg

ABC

In addition you should monitor the Airway, Breathing and Circulation vigilantly, particularly the airway. Start the patient on 15L high flow oxygen as soon as they begin seizing. Put a sats probe in place to monitor O2 saturations. Attempted to gain IV access.

If the seizure persists despite the above measures, then you will need to secure the airway via intubation. This should only be done in a critical care settings (e.g. Emergency Department, HDU, ICU), and you should sedate the patient as you would for any other intubation. This is usually done in the form of a rapid sequence induction, which involves a strong seating agent (e.g. propofol 20mg/Kg Iv), and a paralyzing agent (e.g. sexamethonium 2mg/Kg IV).

Propofol is also an acute antiepileptic. Once the patient has been sedated and paralyzed it is not possible to tell if the seizure has been terminated without the use of EEG monitoring. Ensure the patient has EEG monitoring to check on progress of the seizure.

Once the airway is secured and you have carried out the above measures, seek expert help (e.g. call neurologist).

Third line measures

The following may be attempted if the seizure continues

• Further dose of midazolam
• Further dose phenytoin up to a total of 30mg/Kg
• Thiopentone / profol infusion (likely to require intubation and possibly vasopressor support)

Try to find a cause and treat any underlying factors.

References

• Murtagh’s General Practice. 6th Ed. (2015) John Murtagh, Jill Rosenblatt
• Oxford Handbook of General Practice. 3rd Ed. (2010) Simon, C., Everitt, H., van Drop, F.
• Beers, MH., Porter RS., Jones, TV., Kaplan JL., Berkwits, M. The Merck Manual of Diagnosis and Therapy

Read more about our sources

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