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Case presentation Mr. Golf Unknown

Case presentation Mr. Golf Unknown. Critical Care Academics 11 February 2013. 28 Year male, community assault- pt put alight and assualted with sjambok Injuries include: 30% , 3 rd degree burns to face, abdomen, chest, arms, legs + inhalation burns(soot in mouth)=total of 40%

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Case presentation Mr. Golf Unknown

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  1. Case presentationMr. Golf Unknown Critical Care Academics 11 February 2013

  2. 28 Year male, community assault-pt put alight and assualted with sjambok • Injuries include: • 30% , 3rd degree burns to face, abdomen,chest, arms, legs + inhalation burns(soot in mouth)=total of 40% • Bilateral mandible fractures, subdural- and subarachnoid hemorraghes and cerebral oedema • Diffuse soft tissue injuries with rhabdomyolyis

  3. i Examination on admission Vital signs: • BP: 113/89mmHG • Pulse: 119 b/min • Temp: 35° • RR : 22b/min • Pulse Oximetry: 98%

  4. Physical examination - GCS 7/15 (E1 M5 V2), pupils dilated but reactive • Abdomen: no signs of acute abdomen or injury • Resp: no signs of resp compromise/distress (intubated due to low GCS and inhalation burns) • 30% burns arms, legs, abdomen, face

  5. Biochemistry: • Sodium: 139 mmol/l • Potassium: 3,8 mmol/l • Chloride: 105 mmol/l - Urea: 5,6 mmol/l • Creatinine: 124 mmol/l • Myoglobin: 2322 uq/l • CK: 4052 u/l • CK-MB: 48,9 ug/l • Trop I: 71ng/

  6. - HB: 13,8 g/dl • WCC: 10, 42 • Platelets: 404 • CRP: 138 ng/l • INR 1,53 • PCT 7,9 ug/l

  7. Arterial bloodgas • pH : 7,45 • paO2 : 133,7mmHg • paCo2 : 40,0 mmHg • P/F ratio : 232 mmHg • SaO2 : 98% • HCO3 : 20,9 mmol/l • Lactate : 4.0 mmol/l

  8. Patient intubated and ventilated in casualty-SIMV (vol control) • Myoglobin regime initiated 6 hours post injury • FAST –no free fluid, no abdominal pathology • Fluid resuscitation acc to Parkland formula (4ml/kg/% burns) • Admitted to SICU 12 hours post-injury

  9. Progress in SICU • Extradural ICP monitered=25 mmHg, pt sedated and paralysed, anti-convulsants started • Early enteral nutrition initiated • Wounds cleaned and dressed with Flamazine • Day 4 post admission- new opacification + pleural effusion left lower lobe+ pyrexia • WCC decreased to 0,38, CRP 304, PCT 4,5 • Confirmed HIV + status • Haemodynamic instability-vasopressor support required • Severe sepsis , septic burns to lower limbs

  10. Below-knee R + forefoot amputation L doneto obtain source control • Pseudomas, coagulse- Staph cultured on LUKI, yeast on CVP • Meronem, Teicoplanin , Colistinstarted, Amphotericin B added later • No response after days, still severe LRTI-necrotising pneumonitis, pneumothorax developed and ICD placed

  11. Currently: • Day 11 Meronem+Teioplanin +Colistin, Amphotericin B day 6, necrotising pneumonitis-minimal response, still septic, deranged LFT’s • Minimal neurological improvement - GCS=5/10 (M4, E1) • Still ventilated, haemodynamically unstable, pyrexial

  12. Arterial blood gas - ph: 7,41 - FiO2:40% - P/F ratio: 186 - PaO2: 74 - PaCo2:36 - HCO3: 23 • HB : 8,7

  13. - BE: -1,5 - lactate: 1 • Bili total: 26 • Biliconj: 16 • Alb<10 • GGT: 253 • ALP: 156 • ALT: 159 • AST:338

  14. Biochemistry • Na: 137 • K: 4,2 • Cl: 106 • Urea: 5,2 • Creatinine: 49 • WCC 5,36 • PCT 3,6 • CRP 217 • INR 1,49

  15. Endpoints of discussion • Fluid resuscitation/ management of burns patient • Pathophysiology of rhabdomyolysis • Myoglobin regime • Management of severe head injury • Nutrition in critical care- severe head injury and burns

  16. Rhabdomyolysis Rhabdomyo = striped muscle Lysis = dissolution

  17. Causes • Trauma • Exertion • Hypoxia • Genetic defects • Infections • Body temperature changes • Metabolic and electrolyte disorders • Drugs and toxins • Idiopathic

  18. Rhabdomyolysis Rhabdomyo = striped muscle Lysis = dissolution

  19. Causes • Trauma • Exertion • Hypoxia • Genetic defects • Infections • Body temperature changes • Metabolic and electrolyte disorders • Drugs and toxins • idiopathic

  20. Causes • Trauma • Exertion • Hypoxia • Genetic defects • Infections • Body temperature changes • Metabolic and electrolyte disorders • Drugs and toxins • idiopathic Burns

  21. Most serious complication : AKI Rhabdomyolysis + AKI : 59 percent † Rhabdomyolysis – AKI : 22 percent † AKI KILLS

  22. Pathogenesis of AKI in rhabdmyolysis • Renal vasocontstriction • volume depletion: due to fluid sequestration damaged muscle • Vascular mediators released from muscle. • Tubule obstruction • Myoglobin – Tamm Horsfall complex in acidic conditions • Direct toxicity • Myoglobin contains Fe2+, which forms free radicals in in conditions of rhabdomyolysis.

  23. Treatment Start/Stop:Bosh et al. NEJM july 2009 • When to treat? • Use plasma CK. Do not use plasma Myoglobin. • No consensus about CK cutoff : 15000IU ? • Take other factors into acount : CRF, sepsis, ... • What about myoglobinuria as a marker? • When to stop treating? • Upon disappearance of myoglobinuria. • No CK or myoglobincutoff values discribed in current literature.

  24. Treatment / Prevention • Renal vasocontstriction • volume depletion: due to fluid seaquestrationin damaged muscle • Vascular mediators released from muscle. • Tubule obstruction • Myoglobin – Tamm Horsfall complex in acidic conditions • Direct toxicity • Myoglobin contains Fe2+, which forms free radicals in in conditions of rhabdomyolysis.

  25. Treatment / Prevention • Renal vasocontstriction • volume depletion: due to fluid seaquestrationin damaged muscle • Vascular mediators released from muscle. • Tubule obstruction • Myoglobin – Tamm Horsfall complex in acidic conditions • Direct toxicity • Myoglobin contains Fe2+, which forms free radicals in in conditions of rhabdomyolysis.

  26. Treatment of volume depletion • Early and agressive volume replacement • Only retrospective data, Shimazu et al. , Gunal et al. • ... but expert consensus. • What fluid? • Studies only done with saline and ringers. • Ringers group needed more HCO3- (Cho et al.) •  consensus to use saline • What is agressive? • Very vague recommendations (NEJM july 2009) : • On average 400cc / h • 200 – 1000cc / h depending on setting and severity • While monitoring hemodynamic status • Target urine output of 3 ml / kg

  27. Treatment / Prevention • Renal vasocontstriction • volume depletion: due to fluid seaquestrationin damaged muscle • Vascular mediators released from muscle. • Tubule obstruction • Myoglobin – Tamm Horsfall complex in acidic conditions • Direct toxicity • Myoglobin contains Fe2+, which forms free radicals in in conditions of rhabdomyolysis.

  28. Treatment of acidosis: NaHCO3+? • No Evidence based proof for this practice (Homsi et al., Brown et al.) • ... But attractive rationale • No Tamm Horsfall – myoglobin complex formation • Prevents redox reactions • Prevents vasoconstriction due to methemoglobin • Counteracts saline hyperinfusion acidosis • Recommendation : (NEJM 2009) • If urinary pH < 6.5 alternate saline with saline + 100mmol NaHCO3+ • Stop if no effect on urinary pH in 4-6h

  29. Treatment / Prevention • Renal vasocontstriction • volume depletion: due to fluid seaquestrationin damaged muscle • Vascular mediators released from muscle. • Tubule obstruction • Myoglobin – Tamm Horsfall complex in acidic conditions • Direct toxicity • Myoglobin contains Fe2+, which forms free radicals in in conditions of rhabdomyolysis.

  30. Flushing away the obstruction? • Volume repletion !! • Diuretics • Mannitol : • No evidence based proof (Homsi et al, Brown et al.) • ... But attractive rationale • Prevents hypovolemia (‘draws sequestrated fluid back in circulation) • Free radical scavenging effects • Flushing effect • Recomendation (NEJM 2009): consider mannitol • Lasix: • Only flushing effect • No evidence based proof • Recommendation: (NEJM 2009) use only if indicated due to other reasons than rhabdomyolysis.

  31. Treatment / Prevention • Renal vasocontstriction • volume depletion: due to fluid seaquestrationin damaged muscle • Vascular mediators released from muscle. • Tubule obstruction • Myoglobin – Tamm Horsfall complex in acidic conditions • Direct toxicity • Myoglobin contains Fe2+, which forms free radicals in in conditions of rhabdomyolysis.

  32. Antioxidants • Pentoxyifilline, Vitamin E, Vitamin C • Case reports, case series, in vitro studies • May be justified, but not enough evidence. (Vanholder et al, Huerta et al)

  33. Treatment overview • Early and agressive volume replacement with saline. • Average 400cc/h • Target urinary output : 3cc/kg/h • Monitor hemodynamic status • Add HCO3- if urinary pH < 6.5 • Consider mannitol • In case of Hyperkalemia, oliguria, volume overload, metabolic acidosis  dialyse (with high flux filter?)

  34. Treatment pitfalls • Late treatment, underresuscitation • Overresuscitation , especially in anuric/oliguric patients. • Hyperkalemia

  35. Take home message SBAH • Resuscitate early and aggressively. • ... but don’t get carried away either,  if patient is anuric or oliguric, don’t drown the patient and call the nepfrologist. • Do not use myoglobin, Use CK. • Check electrolytes.

  36. Resuscitation of the Burns Patient • Initial Assessment and Treatment • Airway Management • Fluid Resuscitation • Wound Management • Secondary Survey • Complications

  37. Initial assessment and treatment • Initial treatment and assessment occurs simultaneously with resuscitation. • Primary management includes stabilizing airway +C-spine, assess for inhalation burns, ?resp distress, ?intubation , breathing, circulation (ABCDE). • Add algorithm

  38. Fluid resuscitation • Rapid, aggressive fluid resuscitation to -reconstitute intravascular volume -maintain end-organ perfusion • Determine fluid requirements by considering following: • Age • Severity of burns-depth and percentage burns • Co-morbidities • Associated injuries

  39. Parkland formula • Fluid requirements in first 24 hours= 4ml/kg body weight for each % TBSA (superficial burns excluded) • Adapt formula to personal requirements: 2-4ml/kg body weight for each% TBSA as this pt was fluid overloaded • First half given over initial 8 hours • Second half given over following 16 hours • Choice of fluid- crystalloid in form of RL- colloids and hypertonic saline not advised • Step down to 5%dex, 0,45% saline with 20mEq KCL in each vacoliter when adequate resus achieved. • Blood transfusions not advised if HB > 8mg/ dL (with transfusion threshold of 10mg/dL). In this case not indicated.

  40. Monitor fluid status • NB!!!! Confirming adequate resus response, more important than adherence to Parkland formula( in this case myglobin regime +fluid resus should’ve been adapted to pt’s fluid requirements) • Maintain urine output at 0,5ml/kg/hour • Clinical signs of volume status -pulse rate <110b/min (normovolemia), > 120b/min (hypovolemia) -distal pulses -pulse pressure -straight-leg-rise test etc. -vigileo, venous sats, serum lactate levels • Monitor hourly for first 24 hrs and ADJUST ACCORDINGLY!!! • PREVENT OVER-RESUSCITION!!!!!! increased incidence of compartment syndromes, pulmonary oedema etc.

  41. Immediate wound care and cooling Pain management • Intravenous morphine advised • Consider benzodiazepines in severe anxiety

  42. Second survey and management • Laboratories- FBC,U+E, glucose, venous blood gas, ABG, CXR, Myoglobin levels, CK, serum lactate levels • Tetanus immunization • Topical antibiotics-silver sulfadiadize most commonly used • Wound management-irrigation soap + water, debridement, • Metabolism/nutrition -Start feeding as soon as resus underway (increased wound healing and shorter hospitalization) -Glucose monitoring (strict glucose control @ 8-10mmol/l) -Anabolic steroids • Modulating catabolic response • Glycemic control( 8-10mmol/l) • Beta blockers

  43. Preventable complications • Hypothermia • Compartment syndromes • In this case PULMONARY OEDEMA! • DVT-routine thromboembolic prophylaxis • Heparin-induced thrombocytopenia • Stress ulcers-routine prophylaxis • Adrenal insufficiency

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