wellen's syndrome

High risk Ecg changes- need admission under cardiology (via medics) even if pain free een if normal troponins. 


Diagnostic criteria (from LITFL):

•Deeply-inverted or biphasic T waves in V2-3 (may extend to V1-6)

•Isoelectric or minimally-elevated ST segment (< 1mm)

•No precordial Q waves

•Preserved precordial R wave progression

•Recent history of angina

•ECG pattern present in pain-free state

•Normal or slightly elevated serum cardiac markers

High Performance CPR

Whilst listening to a recent podcast on the arguable use of USS in cardiac arrest, the topic of high performance CPR was brought up. Here is a summary of the guidelines and why they are so important:


Four key components of high performance CPR:

  1. CPR rate of 100-120/minute (ideally 110)
  2. Depth at 2-2.5 inches/ 5-6cm
  3. Full recoil (no leaning)
  4. Minimise the pauses whilst rotating compressor every 2 minutes


Why is continuous, good CPR so important?

The aim of CPR is to restore blood flow around the body, keeping organs functioning to reduce morbidity and mortality after cardiac arrest (1)

  • Overall prolonged pauses are associated with increased mortality (2)
  • Adequate coronary perfusion pressure (CPP) to provide myocardial blood supply is typically 15-25mmHg
  • Adequate CPP is critical to defibrillation success
  • A pause in compressions of 10 seconds results in a CPP drop of 29.8 to 6.8mmHg (77% drop) (3)
  • A pause in compressions of 4 seconds results in a drop of 23.4 to 7.6mmHg (68% drop)
  • The study showed that 83% of a decline in CPP can be restored during a short period of decompressions prior to defibrillation, but compressions need to continue for longer to re-attain the same CPP prior to the pause


Take-away points:

  • Advise a countdown of 5 seconds every pause in defibrillation
  • Questionable use of USS for echo during pauses – but can use the USS over femoral artery to ensure good quality compressions



  • Chest compression pauses during defibrillation attempts. Deakin CD, Koster RW. Curr Opin Crit Care. 2016 Jun;22(3):206-11. doi: 10.1097/MCC.0000000000000310.
  • Association between chest compression interruptions and clinical outcomes of ventricular fibrillation out-of-hospital cardiac arrest. Brouwer TF, Walker RG, Chapman FW, Koster RW. Circulation 2015; 132:1030–1037.
  • Restoring coronary perfusion pressure before defibrillation after chest compression interruptions. Mader T, Coute R, Kellogg A, et al.Open J Emerg Med 2014; 2:29–35


true lateralx-rays

Hand Injuries – True Lateral Xrays


The images below were taken 3/52 apart.


Punch injury, swelling with lateral x-ray (image 1) – diagnosed as base of 3rd MC # and backslab applied and fracture clinic made for 16/7 later.




                        IMAGE 1                                                                           IMAGE 2


Returned to A&E 21 days post-attendance as missed fracture clinic 3-4/7 earlier, requesting POP to be removed – gross deformity and true lateral x-ray (image 2) 

ORIF & k wired the following day





1.   Always make sure if significant injury suspected that you gain a true lateral x-ray

2.   If concerned re # discuss with ED Consultant or ortho that day if fracture clinics

      >1-2/52 later

Staggered Paracetamol Overdose

Staggered Paracetamol Overdose


Updated Toxbase Guidance January 2018

·         Start treatment with acetylcysteine without delay in ALL staggered overdoses- MHRA Advice


·         Check bloods AT LEAST 4 hours after last paracetamol ingestion


·         Check paracetamol levels, U&E, creatinine,  LFTs, INR, bicarbonate(VBG)


·         Clinically significant hepatotoxicity is unlikely if at least 4 hours after last ingestion the following criteria are meet-

o   Paracetamol concentration <10 AND

o   ALT is normal AND

o   INR is ≤ 1.3 AND

o   The patient has no symptoms suggesting liver damage


·         Patients can be considered for discharge if all the above criteria are met and the creatinine is normal


·         If the above criteria are not met then acetylcysteine should be continued as per Toxbase guidance


·         If the creatinine has risen significantly from baseline treat conventionally and recheck in 8-12 hours


·         Patients should be advised to return if they develop vomiting, abdominal pain, jaundice


·         Patients with normal liver function following treatment with acetylcysteine can recommence therapeutic paracetamol

ARDS - Acute Respiratory Distress Syndrome


What is ARDS?


Classified as non-cardiogenic pulmonary oedema

It typically presents within one week of injury

The term 'acute lung injury' has been discontinued in favour of ARDS

It results from bilateral infiltrates in the lung that leads to increased vascular permeability, increased lung dead space and reduced lung compliance, resulting in hypoxaemia


What are the causes?


Infection: pneumonia, aspiration pneumonia

Trauma: massive trauma, inhalation injury, drowning

Other: pancreatitis, transfusion injury, embolism


Why does it matter?


The LUNGSAFE trial identified around 10% of ICU admissions showed ARDS. Despite this the condition is underrecognised by professionals and therefore undertreated

There is a high mortality rate associated with ARDS, increasing with the severity


How is it diagnosed?


CXR - shows bilateral alveolar shadowing

Refractory hypoxaemia: Work out the PaO2:FiO2 ratio

  • In a healthy individual on air the FiO2 will be 21%, the PaO2 between 11-14. Therefore a normal PaO2:FiO2 ratio will be 14/21= 0.66= 66%
  • Stage 1 ARDS is classified by a ratio of <45% (27% mortality)
  • Stage 2 is <30% (32% mortality)
  • Stage 3 is <15% (45% mortality)


How is it treated?


Treat the underlying cause

Position the patient  - the prone position improves oxygenation and mortality in ARDS

Use PEEP - set a tidal volume of 6ml/kg of predicted body weight. Set the respiratory rate to maintain optimal mechanical ventilation (not greater than 35 resps per minute). Target sats >90%

Get ITU involvement early




High mortality

Good outcome at 6 months for survivors

May suffer from a reduced quality of life due to hypoxia induced cognitive impairment, depression and PTSD







Epidemiology, Patterns of Care, and Mortality for Patients With Acute Respiratory Distress Syndrome in Intensive Care Units in 50 Countries. Giacomo Bellani, MD, PhD1,2; John G. Laffey, MD, MA3,4; Tài Pham, MD5,6,7; et al;  the LUNG SAFE Investigators and the ESICM Trials Group. JAMA. 2016;315(8):788-800. doi:10.1001/jama.2016.0291

What on earth is a BRUE?

BRUE - Brief Resolved Unexplained Event


Previously known as ALTE

Includes - apnoea; colour change (including red); floppy; stiff; choking

Airway reflex - apnoea - pale/floppy

95% benign but 1% mortality

Low risk:

·     >60 days old

·     >32/40

·     1 event

·     No CPR (medical professional)

·     Nil Concerning


·     Related to NAI

·     Sweating with feeds suggest cardiac pathology

·     Increase yield of investigation if - >1 episode; premature; blood in nose


·     Share decisions

·     CPR training for parents

·     Consider pertussis swab/ECG

·     Consider brief period monitoring

·     Should not do bloods; LP; CXR; ECHO; EEG; empirically treat reflux

·     Need not do viral swabs; urine; glucose; gas


Advise admit to paeds for observation and reassurance to parents

Fever in the returning traveller

With travel abroad for business or leisure on the increase, exposure to pathogens not native to the UK need to be considered, especially when presenting with fever. 


Specific points to consider - History

·        Symptoms, including time of onset

·        Where travelled to and timings stayed in each place.

·        Any pre-travel preparations/immunisations/medication taken

·        Known insect bites

·        Exposure to local population

·        Food and or/drink consumed whilst abroad

·        Activities undertaken whilst there (see table 1) and/or any potential sexual exposure.


Table 1 Infections associated with specific activities


Possible causes of fever

Work in hospitals or refugee camps

Tuberculosis, HIV, viral haemorrhagic fever (VHF), typhus

Sexual exposure

HIV, hepatitis B and C, syphilis, gonorrhoea

Visit to African game park

Tick typhus

Fresh water exposure

Schistosomiasis, leptospirosis


Histoplasmosis, rabies

Contaminated food and water/raw meat or fish

Enteric fever, Shigella, Salmonella, Campylobacter, amoebiasis, helminth infections, hepatitis A and E

Ingestion of unpasteurised milk

Brucella, Listeria, Salmonella

Animal contact

Brucella, Q fever

Air conditioning systems, showers






Specific points to consider – Examination

Full examination, specifically noting the following features associated with a specific pathogen:

·        Jaundice – viral hepatitis, leptospirosis

·        Maculopapular rash – Dengue, HIV, syphilis, typhus, chikungunya

·        Eschar – Typhus

·        Urticarial rash – Acute schistosomiasis (Katayama fever), strongyloids

·        Bloody diarrhoea – Shigella, Salmonella, amoebiasis

·        Hepatomegaly – Enteric fever, leptospirosis, viral hepatitis

·        Splenomegaly – Malaria, visceral leishmaniasis


Specific points to consider – Investigations

·        FBC, U+Es, LFTs

·        3 x malaria blood films

·        Blood cultures

·        HIV tests

·        Urine and stool cultures and microscopy

·        Chest x-ray and USS liver and spleen

·        Serology +/- polymerase chain reaction (PCR) for dengue and other arborovirus infections, rickettsiae, Q fever, Brucella



Table 2 Disease by incubation period


Incubation period



(<10 days)

•   Arboviral infections (dengue, chikungunya)

•   Gastroenteritis, acute (bacterial, viral)

•   Relapsing fever (borrelia)

•   Respiratory infection (bacterial, viral)

•   Rickettsial infection (eg, typhus, Rocky Mountain spotted fever)

•   Malaria (Plasmodium falciparum, 6-90 days, usually <30 days)

•   Lassa fever, Marburg virus

•   Ebola virus (2-12 days)

•   West Nile virus

•   Cholera

•   Plague

•   Yellow fever (3-16 days)

•   Influenza

•   SARS

(10-21 days)


•   Brucellosis

•   Enteric fever (typhoid and paratyphoid)

•   Leptospirosis

•   Melioidosis

•   Q fever (Coxiella burnetii)

•   Ebola virus


•   Coccidioidomycosis

•   Histoplasmosis

•   Chagas' disease, acute

•   Malaria (P. falciparum)

•   Trypanosoma brucei rhodesiense (East African/Rhodesian African sleeping sickness)


•   Cytomegalovirus (CMV), Epstein-Barr virus (EBV), HIV

•   Viral haemorrhagic fever

•   Yellow fever



(>21 days)


•  Brucellosis

•  TB


•  Schistosomiasis (acute)


•  Amoebic liver abscess

•  Malaria (including P. falciparum)

•  Trypanosoma brucei gambiense (West African/Gambian sleeping sickness)

•  Visceral leishmaniasis


•  HIV, viral hepatitis

•  Rabies (up to one year)



Resources for further information and disease risk by country:







1.      Bell DJ. Fever in the returning traveller. J R Coll Physicians Edinb 2012; 42:43–6 © 2012 RCPE

2.      Lowth M. Diagnosing the Tropical Traveller.  Accessed at http://patient.info/doctor/diagnosing-the-tropical-traveller (accessed 1 May 16)

  1. National travel Health Network and Centre: www.nathnac.org
  2. Travax: A–Z of healthy travel: www.travax.nhs.uk
  3. HPA Migrant Health Guide: http://www.hpa.org.uk/MigrantHealthGuide