On the 9th January 2018 an investigation was commenced into the death on the 26th December 2017 of Christian James Gabriel Hobbs (aged 17 years). The investigation concluded at the end of the inquest on the 14th October 2024 and some key determinations were :- Medical Cause of Death : 1a. Multi Organ Failure 1b. Cardiogenic Shock 1c. Arrhythmogenic cardiomyopathy Conclusion: Died from complications following an acute deterioration having decompensated over a short period of time on a background of a previously undiagnosed pre-existing arrhythmogenic cardiomyopathy.

1. Christian had no known relevant past medical history. He was at school and had a passion for and love of boxing from a young age. He was a member of a boxing club. His father, who had served for 10 years as an infantry officer in the Army said that he had seen fit men, but Christian was amongst the fittest he had seen.
2. The Christmas period in 2017 had led to a large gathering at the family home in Northamptonshire. On Christmas day, Christian seemed fine before lunch and a photograph had been taken. He was said to have been in good form over lunch but went inside as he was not feeling well. It was not considered that he had anything other than a suspicion of flu.
3. When checked the following day, he seemed much the same at circa 12 noon and he was adamant he still wanted to go on holiday. He had taken paracetamol and Ibuprofen. He was checked again in the late afternoon and his mother then asked his grandfather (a retired Consultant) to look at him because of some concerning features. His grandfather found his conscious level to be ‘tenuous’. He considered him to be clammy and shut down. The radial pulse was not palpable and the carotid pulse was circa 240. He considered Christian was morbidly white and had no capillary return.
4. As a result, Christian’s parents urgently transported him by car to the City Hospital, Peterborough. Christian told his mother on the journey that his heart had been going fast since after lunch the previous day and had a sound of rushing blood in his ears like he had been on a long run.
5. His grandfather telephoned the hospital and spoke to a receptionist and pre-warned about his arrival and relayed concerns about the heart rate, the poor perfusion and ‘the prejudiced cardiac output’. ADMISSION TO PETERBOROUGH CITY HOSPITAL 26/12/2017
6. Christian was documented as having arrived in the Emergency Department (ED) at 17:42.
7. Christian was seen by the assessment nurse on recorded entries at circa 17:45 where the presenting complaint was documented as?AF/?SVT. It was also documented that Christian had complained of chest tightness and vomiting and that he had already taken paracetamol and ibuprofen.
8. Observations documented a heart rate of 159 (with a recorded entry of 240 also), a blood pressure of 91/71 respiratory rate 17, SpO2 100% and Glasgow Coma Score 15. It was documented that Christian ‘looks pale’. Christian was triaged using the Manchester Triage System as category 2.
9. A plan was made for ongoing observations, an ECG, bloods and IV fluids. Only the observations and ECG were ticked as having been done.
10. Christian was moved into the resuscitation area of the ED, together with his parents. He was in a wheelchair.
11. The first set of observations were documented at 18:00. These recorded a respiratory rate of 25, SpO2 97 on air, temperature 35.9C, blood pressure 79/46, Alert on the AVPU scale.
12. The NEWS score was 10.
13. It was documented that the observations should be continued at 30-minute intervals.
14. The first ECG was done at 18:07.
15. A nurse was involved in care in the resuscitation room together with an ST3 Doctor with the latter recording a number of entries in the notes from circa 18:10 onwards when the assessment was undertaken.
16. The presenting problem was documented as cough, raised temperature, palpitations.
17. The history included:  Unwell since yesterday morning  Felt palpitations while having lunch  In the night developed cough, productive of white phlegm  Had raised temperature and took paracetamol and ibuprofen  Body ache and three episodes of vomiting  Chest tightness but no pain  SOB at times
18. It was also documented that there was no nasal discharge or blockage, no sore throat, no rashes or neck pain, no abdominal pain, and no sudden change in bowel habit.
19. Those observations were recorded as per the observations done at 18:00. In addition, Christian was documented as being dehydrated ++. The pulse was documented as regular with normal heart sounds and the chest was clear with no increase in respiratory effort. The abdomen was soft and non-tender. Christian was not delirious, the GCS was 15, and neurological examination was normal.
20. The working diagnosis was noted as ? sepsis ?chest infection ?viral.
21. The management plan was:  ECG (this was done at 18:07 - described as sinus tachycardia).  Bloods – VBG, cultures  CXR  Urinalysis (a dipstick of the urine to look for signs of infection etc).  IV fluids  Antibiotics  TCI (meaning to come in) under medics if required.
22. The assessment was noted as completed at 18:35.
23. An x-ray was undertaken at circa 18:55
24. Normal saline 1L (an intravenous fluid) and co-amoxiclav 1.2g were prescribed at 18:30 and were documented as started/given at 19:00.
25. Further observations documented at 18:30 reported respiratory rate 23, SpO2 96% on air, temperature 35.6, BP 94/43, heart rate 143, alert. The NEWS score was 8. It was documented that 30-minute observations should continue.
26. At 19:00, cyclizine 50 mg (an anti-sickness drug) was prescribed and this was documented as being given at 19:20.
27. There was a change of shift at 19:00.
28. A nursing handover was recorded - 19:25.
29. Multidisciplinary documentation at 19:35 reported that .. ‘pt looks pallor & presenting as acutely ill. BP↓& tachycardic. Tx underway.’
30. At 19:50, it was documented ‘Struggling to get venous bloods’ and at 20:00 ‘Arterial bloods taken’.
31. An arterial blood gas result recorded at 19:44 showed a pH 7.409, PaCO2 3.1kPa , PaO2 9.88 , HCO3 14.3 mmol/L , BE -7.9 , K+ 5.72 , lactate 5.6 mmol/L.
32. Bloods were received at the haematology laboratory at 20:07 (taken at 19:50), and the clinical chemistry laboratory at 20:13.
33. Observations documented at 20:00 respiratory rate 30, SpO2 100% on air, temperature 36.2, BP 83/?56, heart rate 141, alert, blood sugar 5.6 and a NEWS of 9. Nursing documentation at 20:00 stated ‘No change to pt [patient] condition’.
34. At around 20:15 it was documented that ‘mother called for help – pt agitated
-? Peri-arrest then started agonal breathing.’
35. Retrospective notes written at 20:30 by a medical registrar documented:  Patient suddenly started gasping and not responding at around 20:00  ED team attended – no pulse  Pads attached; polymorphic VT noted.  CPR started, 150J shock given, CPR continued  ROSC , lasted for few ? min  Again lost pulse, CPR started  ROSC obtained  Magnesium infusion + amiodarone infusion started [MgSO4 2g (8 mmol) is documented as given at 20:20, amiodarone 300 mg is documented as given at 21:07]  Decision to intubate made by ED Consultant  Intubated under sedation
36. Retrospective notes written at 20:30 by an ST6 EM documented that they attended a peri arrest buzzer and that the patient was in cardiac arrest and that CPR was in progress. The ED/ICU Consultant was leading. The ST6 EM managed the airway and intubated the trachea uneventfully.
37. Haematology results were reported at 20:22 – the only abnormality being a raised white cell count of 16.4 (monocytes 1.1, neutrophils 13.1).
38. A second ECG was done at 21:09. On it was documented ‘SR (sinus rhythm)’.
39. Clinical Chemistry results were reported at 21:08 and were phoned through to ED. A call from the lab was documented at 21:20: sodium 13, potassium. 6.5, creatinine 115
40. Other abnormalities on the clinical chemistry were, a raised lactate (4.7 mmol/L), raised urea (10.5 mmol/L), raised CRP (44 mg/L) and a slightly raised ALT (64 U/L). Of note the troponin T was raised at 118 ng/L.
41. An ABG taken at 21:15 showed a severe mixed respiratory and metabolic acidosis (pH 6.97, PaCO2 8.52, BE -17.6, lactate 8.7) and a raised potassium (5.23). The PaO2 was 27 on 80% oxygen.
42. Christian had a urinary catheter inserted.
43. A second chest X-ray was done at ~ 20:48.
44. An ABG taken at 21:51 showed an ongoing severe lactic acidosis (pH 7.1, BE
-4.2, lactate 10.3). The PaO2 was 14.56 on 21% oxygen.
45. A third ECG was done at 22:06
46. An ABG taken at 22:21 showed lactic acidosis (pH 7.05, - 16.3, lactate 11.2). The PaO2 was 12.43 on 21% oxygen.
47. Retrospective notes by the ED consultant at 23:35 documented:  Responded to cry for help – parents in resus  Patient had suddenly become unresponsive and started gasping  Agonal respiratory effort  HR 192 regular on monitor – palpable pulse  Oxygen applied followed by resp arrest  BVM and pads  VF on monitor and no pulse  Shock x 1 followed by CPR  ROSC – tachy then VT with pulse followed by PEA arrest [pulseless electrical activity]  CPR for less than one minute before signs of life. Patient moving arms  HR 154 SVT SBP 111 GCS 4 (E1V1M2) . Minimal respiratory effort.  I+V  Hypotensive despite IV fluids (2L) and metaraminol boluses (a vasoconstrictor drug that is used to raise the blood pressure – a total of 9.5 mg was given between 20:25 and 21:05).  Amiodarone and MgSO4 infusions (anti-arrhythmic drugs) (MgSO4 2g (8 mmol) is documented as given at 20:20, amiodarone 300 mg is documented as given at 21:07)  Ceftriaxone given (? Meningoccal sepsis) 2g documented as given at 21:40]  L femoral CVC placed.  Noradrenaline infusion commenced. R femoral arterial line placed  ICU consultant present.
48. Bedside echo by an ICU consultant and also another clinician showed septal wall akinesia. IVC filled.
49. BP remained 80 systolic despite increased noradrenaline (1 g/kg/min). Hydrocortisone 100 mg documented as given at 21:00. Dobutamine 30 mL/hr commenced as started at 21:45.
50. In addition, it was documented that terlipressin 0.5mg was given at 21:55 and that actrapid 10u/50 mL 50% glucose was given but no time was provided.
51. A further litre of normal saline was documented as being given at 21:10.
52. Worsening ABGs: 100 mL 8.4% NaHCO3 , 10 ml 10% calcium gluconate is timed as given at 21:25.
53. ECG ? Brugada
54. A tertiary hospital Cardiology SpR was informed about possible salvage ECMO
55. The systolic BP dropped to 60 mmHg and boluses of adrenaline (total of 400g given between 22:09 and 22:18) were given without response. An adrenaline infusion was started at 22:18
56. A calcium chloride infusion was started at 22:35
57. Observations at 22:25 recorded BP 50/31 and HR 108
58. The blood pressure remained low (systolic blood pressure < 50 and the lactate continued to increase (11.2 on ABG done at 22:21).
59. Observations at 22:45 recorded BP 68/40 and HR 135.
60. Christian was increasingly mottled, worsening gas exchange – likely due to poor perfusion.
61. He was mainly unsedated throughout and no further muscle relaxants since RSI.
62. A call was made to a transplant fellow at a tertiary hospital – the response was, ‘unsure if can help, will speak to consultant’
63. There was a discussion with the tertiary hospital ICU consultant who said, ‘No one is entirely sure what the aetiology is. It is therefore very difficult to know what can be reversed by ECMO, and it is unlikely to be tolerated. Given the prolonged period of hypotension and lack of reversible cause which we can further improve, there is nothing more that can be done’.
64. This was discussed with the family, and it was agreed to stop active treatment and allow him to die which was documented at 23:45.
65. An independent expert report opined that when Christian was first assessed in ED, the symptoms were non-specific (palpitations, chest tightness, cough, aching, vomiting) but there were several concerning observations indicating severe illness. These included:  Tachycardia (fast heart rate) with the lowest rate being 132 and rates of up to 240 documented (a rate that is non-physiological and indicative of an arrhythmia – abnormal heart rhythm).  Hypotension (low blood pressure)  Tachypnoea (fast respiratory rate)  Hypothermia (low temperature)  High NEWS score (8-10)  Looking pale [documented by triage nurse and resus practitioner]  Dehydrated ++ was documented at the first medical review.
66. The expert felt that it was appropriate that Christian was moved into the resuscitation area of the ED where he could be continuously monitored and where there is a high staff/patient ratio.
67. The NEWS score of 10 required the triggering of a clinical response (as documented in the Emergency Department Majors proforma):  The medical review at 18:10 was reasonably comprehensive but missed several key points including:  There was no reference to the heart rate of 240 that was documented in the Doctors notes. It is likely that these arrhythmias were ventricular tachycardia.  It was not documented whether Christian had been passing urine normally.  The capillary refill time and the strength of the peripheral pulses were not documented, a short capillary refill time and bounding pulse may have more in keeping with sepsis, and a slow capillary refill time and weak pulse would have been more in keeping with a low cardiac output state from either hypovolaemia (reduced blood volume) or reduced cardiac contractility.  The jugular venous pressure (JVP) was not documented (a sign of central venous filling pressures and cardiac function).  The ECG was documented as sinus tachycardia. I accepted the evidence of a number of experts that this was not a normal ECG and that there were other non-specific abnormalities.  It was considered that the non-specific abnormalities could be seen in conditions such as hyperkalaemia [high potassium levels] and cardiac dilatation.  A chest X-ray was requested but the results of this were not documented.  In the opinion of the expert ICU consultant, the CXR showed some soft ground glass opacification (GGO), mild upper lobe diversion (increased blood flow to the upper parts of the lung because of increased left sided heart pressures), and some fluid in the horizontal fissure (fluid outside of the lung sitting between the upper and middle lobes) – all these are consistent with heart failure, but they are not specific. In his opinion, these were quite subtle signs and could easily be missed. A retrospective review by a specialist forensic radiologist was clear on the presence of cardiomegaly on the imaging.  Chest sepsis can cause GGO but in the opinion of the ICU expert there was no clear evidence of chest sepsis on the CXR.  The ICU expert did see evidence of some mild pleural fluid in the horizontal fissure.
68. The medical diagnosis was of possible sepsis. I found that it was appropriate to have this high on the list of differential diagnoses as although the presentation was not classic, sepsis can present in many ways and a high index of suspicion is required.
69. However, I did find that it should have been immediately recognised that Christian was in a shocked state from his tachycardia, hypotension, and poor perfusion.
70. When a patient presents with undifferentiated shock (unclear cause), I concurred with the expert evidence, that it is important to immediately initiate therapy whilst rapidly trying to identify the aetiology so that definitive therapy can be administered.
71. I again agreed that it should be expected that any clinician would rapidly treat and investigate the cause of the shock and to regularly reassess to determine the response to treatment and to review the results of investigations. This would need discussion with Senior staff. There was a discussion between the ST3 and the ED consultant but the information exchange did not lead to a consultant face to face assessment of Christian prior to his arrest.
72. The differential diagnosis was not broadened prior to the cardiac arrest.
73. I agreed that it could be expected that a clinician should have recognised that Christian was acutely unwell.
74. As part of the rapid assessment of the aetiology of the shock I concurred with the view that a low cardiac output state ought to have been considered. Because of the probable tachyarrhythmias, the abnormal ECG, the tachycardia and the low blood pressure, cardiac pathology should have been considered. Several entries in the records pointed to Christian being in a ‘shut down’ state (poor peripheral perfusion) – this was documented by the triage nurse (‘looks pale’), the ST3 ED doctor (’dehydrated ++) and the resuscitation room practitioner (‘pallor’, ‘struggling to get venous bloods’). This should have further increased the suspicion of a low cardiac output state.
75. Focused echocardiography was not undertaken and would be a key diagnostic tool, when it is available. It could have answered several simple questions such as:  Is the heart dilated?  Is the heart contracting normally?  Is the heart/circulation well filled?  Is there a pericardial effusion (fluid in the sac around the heart) and if so, is this compromising the heart?
76. An ICU expert was of the opinion that focused echocardiogram should have been done and would likely have shown some abnormalities. An expert Cardiologist also emphasized the importance of this diagnostic tool.
77. It was stated that in sepsis, especially after appropriate fluid challenges, the heart is usually well filled and pumping vigorously on echocardiogram. In cardiogenic shock, the heart function is impaired on echocardiogram and depending on the cause, the chambers may be dilated.
78. The ICU expert indicated that a possible diagnosis of sepsis should have triggered a bundle of assessments/interventions such as the Sepsis 6 bundle. The Sepsis 6 Bundle/Pathway is a series of simple interventions that has been widely used in the NHS since 2007 – it aims to reduce the mortality from sepsis.
79. By the time Christian was in the resuscitation room, he had three ‘Red Flag’ triggers on the Sepsis Screening tool, any one of which should have triggered the Sepsis 6 pathway. The Sepsis 6 pathway includes the following interventions, all of which should be completed within one hour:  Administer oxygen  Take blood cultures, think source control [where is the infection arising from and can the source be controlled]. Chest X-ray and urinalysis.  Give IV antibiotics  Give IV fluids – if hypotensive or lactate >2 then 500 mL stat, which may be repeated if clinically indicated  Check serial lactates – if lactate > 4 mmol/L then call critical care and recheck after fluid challenges  Measure urine output and commence fluid balance chart  If the above interventions do not work or the patient is clearly critically ill, then immediate referral to critical care is indicated.
80. The chest X-ray showed some abnormalities consistent with heart failure; however, there was no handwritten documentation of the time that it was reviewed or what it showed.
81. Intravenous fluids were commenced but these were not given as rapid boluses and targeted against response - Christian remained hypotensive and tachycardic despite the fluid administration.
82. Apart from the blood cultures, bloods were not taken until 19:44.
83. I found that that the urgency of the situation was under-appreciated by the treating team. An expert indicated that it is very well recognised that unwell, and normally fit, children/young adults often look quite well until the point at which they rapidly decompensate. In the experts opinion, the fact that Christian was sitting up and talking resulted in a false sense of security and an under-appreciation of the physiological abnormalities on the part of some of those involved.
84. The expert also opined that there was a clear delay in getting the first blood gas. A cannula was in situ by circa 19:00, when intravenous fluids and antibiotics were given, and a venous blood gas should have been taken from this. This would likely have shown a raised lactate and potassium (as the ABG did at 19:44) – both of which would have impacted on management and should have further highlighted the severity of the situation.
85. I found that if there was difficulty in getting bloods, then this needed to be resolved by deployment of appropriate measures to expedite this.
86. Earlier correction of the high potassium, if it had been measured and recognised, may possibly have reduced the chance of further arrythmias.
87. Cyclizine was given as an antiemetic at circa 19:20. SUBSEQUENT CARE DURING AND AFTER THE CARDIAC ARREST
88. I share the views expressed in written reports and oral evidence that the care given during the resuscitation was generally of a high standard and everything possible was done to restore a spontaneous circulation and to protect organs from damage.
89. Once return of spontaneous circulation (ROSC) had been achieved then it was appropriate to intubate and commence mechanical ventilation.
90. The viewing and findings of the chest X-ray done at 20:48 were not documented.
91. I was of the view that the clinical situation after ROSC was extremely challenging with ongoing shock and hypotension despite multiple interventions. There was significant post cardiac arrest ‘cardiac stunning’ in the context of an already dilated and weak heart from the pre-existing cardiomyopathy.
92. The evidence of fluid management after arrest was hampered by a lack of clarity over timings and the nature of retrospective entries.