PICU

In summary:

ACUTE LIVER FAILURE

ACUTE LIEVR FAILURE è “fulminant  hepatic  failure”                                            

-        A  rare  syndrome  characterised  by  rapid  onset  of  severe  hepatic  dysfunction  in  the  absence  of  pre-existent  liver  disease.

-         In  ALF,  massive  or  submassive  necrosis  of   hepatocytes   causes   impairment   of   hepatic   synthetic  functions  and  development  of  hepatic  encephalopathy.

Acute  Liver  Failure  Study  Group  (ALFSG)  defines  è

-        ALF   in   adults   as   acute   hepatic   dysfunction   (coagulopathy, poor hepatic synthetic function) with development of encephalopathy within 8 weeks.

-        In children, encephalopathy is difficult to  assess,  and  may  not  develop  until  terminal  stages.

-        Hence,  in  children,  ALF  as  defined  by  the  Paediatric  Acute  Liver  Failure  Study  Group  (PALFSG) includes

–No history of known chronic liver disease

–Evidence  of  acute  liver  injury  (increased  liver  enzymes,  hyperbilirubinaemia),  i.e.  evidence  of liver dysfunction within 8 weeks of onset of symptoms

–Coagulopathy   unresponsive   to   vitamin   K  

INR  >1.5  in  patients  with  hepatic  encephalopathy,  or 

INR  > 2.0 in patients without encephalopathy).

Causes è

-        Aetiology  of  ALF  provides  one  of  the  best  indicators   of   prognosis,   and   also   dictates   specific    management    options.   

-        Severity    of    coagulopathy  and  possibility  of  recovery  also  depends  on  the  aetiology.

-        In developed nations drugs account for 70–80% of  the  causative  factors,  whereas  in  developing  nations  idiopathic  and  viral  infections  account  for  the  majority  of  the  aetiological  factors.

Pathophysiology è

-        injury  to  hepatocytes causing  cell  damage  or  cell  death  by  necrosis  or  apoptosis (both may coexist

-        Acute Wilson disease and Reye syndrome àMitochondrial  permeability  is  increased  and  is  associated  with  apoptosis.

-        In  the  early  phase  of  injury  from  warm  and  cold  ischaemia,  hepatocytes  and  endothelial  cells  activate  the  mitochondrial  permeability  transition,  and  mitochondrial  injury  resulting  in  ATP depletion and ensuing necrosis.

-        Necrotic injury of liver cells leads to a loss of cell membrane  integrity  and  eventual  rupture  and  cell  death  with  the  release  of  cytosolic  proteins  - LDH, ALT, AST and ferritin. 

-        Cellular  glutathione  is  diminished,  especially  following   ALF   with   acetaminophen.  à This   increases   cellular   susceptibility   to   oxidative   injury  and  impairs  the  ability  to  conjugate  and  detoxify some toxic substances.

-        Other detoxification  mechanisms  are  impaired, including  the  transport  systems  for  bilirubin,  leading     to     cholestasis     and     conjugated     hyperbilirubinaemia.

-        An important feature is the general loss of Kupffer cell  function  that  results  in  reduced  clearance  of   endotoxin   and   other   substrates   regularly   presented to hepatocytes by means of the portal system, increasing the risk of infection.

-        Site  of  injury  within  the  liver  plays  an  important  role  in  determining  the  ability  of  the  liver  to  regenerate.

Injury  to  the  portal  zone  inhibits  the  regenerative  response,  while 

Injury  to  the  central  zone  with  sparing  of  the  portal zone permits more frequent spontaneous recovery.

-        central   zone   is   more   susceptible   to   ischaemic injury.

Pathophysiological Effects è

• Increased    cardiac    output    with    decreased    systemic vascular resistance

• Increased portal pressure

• Renal vasoconstriction

• Pulmonary shunting; V/Q mismatch

• Total body fluid overload

-        LF  leads  to  the  development  of    severe    systemic    inflammatory    response    syndrome (SIRS) and extensive energy expenditure with catabolism.

-        Rapidly  progressive,  severe  multiorgan  failure  with unpredictable complications such as:

1.    Cerebral  oedema/intracranial  hypertension —varying grades of encephalopathy

2.    Infection—septic shock, peritonitis, etc.

3.    Coagulopathy —GI  bleeds,  mucosal  bleeds,  etc.

4.    Haemodynamics—vasodilatory       shock,       hypovolaemia

5.    Renal    failure—pre-renal    failure,    ATN,    hepatorenal syndrome

6.    Metabolic        concerns—hypoglycaemia,        dyselectrolytaemia

-        Most critical element to patient survival with ALF  is  its  early  recognition.

MANAGEMENT è

-        A multisystem disease with an unpredictable course. 

-        Mortality  in  ALF  is  predominantly  due  to  raised  intracranial  pressure  (ICP),  infections  and   multiorgan   failure.

-        GOAL à Management  of  these  conditions  while  awaiting  recovery  of  liver  function  or  liver  transplantation (LT).

General Measures à

-        Nursed in a quiet environment, preferably in PICU.

-        Put central  venous  line  à  measure  central  venous  pressure,  administer  fluids,  medications  and  blood  products,  and  collect blood samples.

-        Volume   resuscitation   -   aggressively   if   required.  

-        Iv   at  three-fourth  maintenance  requirement.

-        Fluids - glucose based with  a  glucose  infusion  rate  of  at  least  6–8  mg/kg/min.

-         Vasoactive  drugs  such  as  dopamine  and  dobutamine, if  clinically  indicated.

-        Strict intake and output charting should be done.

-        NG tube - feeding/drainage 

-        Urinary   catheter   for   output   measurement.

-        Care  of  bowel,  back,  bladder,  skin  and  eyes  should be done.

-        Following  monitoring  should  be  done: 

(i)             vital  signs,  every  4  hours,  more  frequently  in  an  unstable  child; 

(ii)          neurological  observations/coma  grading,  electrolyte,  arterial  blood  gases,  blood   sugar   and   prothrombin   time   every   12   hours   (more   frequently   in   an   unstable   child); 

(iii)        daily  measurements  of  liver  span  and   prescription   review;  

(iv)         liver   function   tests,  blood  urea,  serum  creatinine,  calcium  and   phosphate   at   least   twice   weekly;   and 

(v)           Surveillance blood and urine cultures during the course of illness.

Aetiology-Specific Therapy è

Paracetamol (Acetaminophen) Poisoning

-        Rummack–Mathew  nomogram may  aid  in  determining   the   likelihood   of   serious   liver   damage,  but  cannot  be  used  to  exclude  possible  toxicity  due  to  multiple  doses  over  time,  when the  time  of  ingestion  is  unknown.

-        Complete  recovery  occurs  with  timely  (started  within  24  hours)  supportive  care  and  N-acetylcysteine (NAC).

-        NAC has   proven   role   in   the   treatment   of   paracetamol  toxicity. 

-        It  should  be  given  as  early  as  possible, but may still be of value 48 hours or more after  ingestion. 

-        Intravenous   administration   (loading   dose   150   mg/kg   in   5%   dextrose,   followed by a continuous infusion at 10 mg/kg/h).

-        Continue  NAC  till  hepatic  function  normalises  (as evidenced by decreasing INR).

-        Oral  charcoal  is  given  if  patient  presents  within  2  hours  of  ingestion.  It  does  not  interfere  with  absorption of oral NAC.

Non–Paracetamol-Induced ALF

-        NAC  is  useful  in  non-paracetamol  ALF  also  (as  it  improves  systemic  haemodynamics  and  tissue  oxygen  delivery).  However, the probability of complete recovery is less than that with paracetamol-induced hepatic injury.

-        Viral  hepatitis  A  (and  E)–related  ALF  must  be  treated  with  supportive  care  as  no  virus-specific   treatment   has   been   proven   to   be   effective. 

-        Nucleos(t)ide  analogues  should  be  considered  for  hepatitis  B–associated  ALF  and  for  prevention  of  post-transplant  recurrence. 

-        Patients  with  known  or  suspected  herpes  virus  or  varicella  zoster  as  the  cause  of  ALF  should  be  treated  with  acyclovir  (5–10  mg/kg  IV  every  8 hours) and may be considered for LT.

-        Patients  in  whom  Wilson  disease  is  the  likely  cause  of  ALF  must  be  promptly  considered  for  LT.  

-        Patients  with  autoimmune  hepatitis  should  be  considered  for  LT  even  while  corticosteroids  are  being administered.

Intensive Care Issues in Acute Liver Failure è

• Hepatic encephalopathy/cerebral oedema

• Infection

• Coagulopathy

• Haemodynamics

• Renal failure

• Metabolic concerns

Hepatic Encephalopathy è

-        Most  serious  and  life-threatening  complication  of  ALF. 

-        Occurrence  of  cerebral  oedema  and  intracranial  hypertension  is   related   to   severity   of   encephalopathy   (risk   of  cerebral  oedema  25–35%  in  Grade  III  HE;  increases to 65–75% in Grade IV).

Pathophysiology of Hepatic Encephalopathy

-        Increased  ICP  is  a  major  cause  of  mortality  in  patients  who  have  ALF. 

-        Hyperammonaemia,  increased  cerebral  blood  flow  and  enhanced  inflammatory   response   play   central   roles.

-        Hyperammonaemia      is      associated      with      increased  levels  of  glutamine  within  astrocytes.

-        Accumulation   of   glutamine   results   in   cell   swelling and brain oedema.

-        Hyperammonaemia alone      does      not      predict      intracranial      hypertension

-        Increased  cerebral  blood  flow  may  contribute  to   the   development   of   cerebral   oedema   by   facilitating   water   movement   down   altered   osmotic   gradients   generated   by   increased   concentration of glutamine within astrocytes.

-        In   addition,   markers   of   inflammation   are   increased   in   ALF,  perhaps   reflecting   the   SIRS.   SIRS   seems   to   result   in   worsening   encephalopathy,  although  its  direct  relationship  to brain swelling is not defined.

-        HE    encompasses    many    neuropsychiatric    disturbances,  ranging  from  minor  confusion  and  disorientation  to  frank  coma,  resulting  in  intracranial hypertension.

Prevention/Management of Cerebral Oedema in ALF

-        • Grade I/II encephalopathy

–Consider transfer to LT centre

–CT brain to rule out other causes of decreased mental status–Avoid sedation/excessive stimulation

–Negative  fluid  balance  as  tendency  to  retain  water

–Antibiotics:  Surveillance  and  treatment  of  infection.   Prophylactic   antibiotics   possibly   helpful if HE rapidly worsening

–Lactulose: Possibly helpful

–No role for l-ornithine–l-arginine)

-        • Grade III/IV encephalopathy

–Neuroprotective care–Intubate and mechanically ventilate

–Negative  fluid  balance  as  tendency  to  retain  water

–Consider  placement  of  ICP  monitor:  Target  therapy    to    maintain    cerebral    perfusion    pressure (CPP)

–Seizure control; role of prophylaxis unclear

–Mannitol   and   hyperventilation   as   rescue   measures only

–Therapeutic hypothermia: Promising results

Controversies  in  the  Management  of  HE/Cerebral  Oedema in ALF

• ICP monitor insertion: An ongoing debate

-        Benefit of ICP monitoring

-        Allows   early   recognition   of   intracranial   hypertension

-        Helps  target  therapy  to  CPP  (CPP  =  MAP  – ICP)

-        Most  useful  in  patients  with  Grade  III/IV  HE

-        Particularly  useful  during  orthotopic  LT  when  shifts  in  haemodynamics  can  cause  large fluctuations in CPP

-        Target  CPP  >45  mmHg  in  infants,  >50–55  mmHg for older kids and > 60 mmHg for adults.

-        Risks of ICP monitoring

-        Intracranial   bleed:   10–20%   depending   on  the  type  of  ICP  probe  used.  Correct  coagulopathy  prior  to  insertion  till  INR  <1.5.  Recombinant  factor  VII  concentrate  (rFVIIa)    may    be    helpful    during    the    procedure of ICP monitor insertion

-        Infection

-        Correction    of    coagulopathy    should    be    continued for about 48 hours after insertion of ICP probe to prevent bleeding.

-        Measures  to  decrease  ammonia:  Serial  trends  of  serum  ammonia  level  important  for  risk  stratification.

-        Serum ammonia > 200 μmol/L are usually associated with herniation

–Drugs used to decrease ammonia level

Non-absorbable  disaccharides:  Lactulose/lactilol

–Acts   as   a   laxative;   decreases   intestinal   absorption of ammonia and glutamine

–Risk of gaseous bowel distension

–Can be given per rectally as enema

–Cannot be used in patient with ileus

–Insufficient evidence of effect

Antibiotics

–Reduces    intestinal    ammonia    production    by      acting      against      urease-producing      microorganisms

–Rifaximin   more   effective   than   neomycin/metronidazole. Less effective than lactulose -Zinc

–Regulation of protein and nitrogen metabolism

–Slow  acting;  more  useful  in  chronic  hepatic  failure

Steroids: No role

Therapeutic hypothermia

–Gaining  acceptance  as  a  measure  to  reduce  refractory ICP in ALF

–Moderate hypothermia (32–34°C)

↓ cerebral metabolism

Suppresses seizures

Normalises cerebral blood flow

↓ delivery of ammonia to brain

↓ oxidative stress to brain

Reversal of SIRS

Infections in ALF

-        • ALF  is  an  immunocompromised  state  due  to  decreased Kupffer cell function. Hence, patients are  prone  to  bacterial  and  fungal  infections. 

-        Common   organisms   include   Staphylococcus, Streptococcus and    GNB.    Broad-spectrum    coverage with a third-generation cephalosporin, vancomycin/teicoplanin   and   fluconazole   is   recommended wherever indicated.

-        • Peripheral  vasodilatation  due  to  ALF  closely  mimics septic shock.

-        • Since  occult  infection  is  a  common  cause  of  worsening encephalopathy, periodic surveillance cultures to detect bacterial and fungal infections as  early  as  possible  should  be  done,  particularly  in patients who are likely transplant candidates.

-        Prophylactic   antibiotics   and   antifungals   are   indicated only if the patient has

–Hypotension

–SIRS with features of sepsis

–Signs of peritonitis

–Progression of encephalopathy

–Surveillance   cultures   growing   significant   isolates

–Waiting for organ transplant.

Correction of Coagulopathy in ALF è

Coagulopathy in ALF

-        • Coagulopathy  is  a  dynamic  marker  of  hepatic  dysfunction.   

-        Risk    of    bleeding    increases    due     to     concomitant     thrombocytopenia,     hypofibrinogenaemia  and  vitamin  K  deficiency. 

-        Vitamin  K  should  be  prescribed  for  all  patients  with  ALF  and  should  be  given  as  an  infusion.

-        • Hallmark: Decreased synthesis of procoagulants

–Impaired anticoagulation and fibrinolysis

–Thrombocytopenia and thrombasthenia

-        • Factor V has prognostic value.

-        • Indications of correction of coagulopathy

–Significant spontaneous bleed

–Prior to invasive procedures

–Profound coagulopathy (INR > 7)

Variceal Bleeding and Haematamesis è

-        Major  gastrointestinal  bleeding  in  the  setting  of  end-stage  liver  disease  and  portal  hypertension  may  occur  because  of  oesophageal/gastric  varices,  portal gastropathy or distal bowel varices.

Management à

-        • Resuscitate with colloid and blood products.

-        • Correct   coagulopathy   (vitamin   K,   FFP   or   cryoprecipitate).

-        • Start  IV  octreotide  or  any  other  octreotide  analogue that is available.

-        • Perform   gastroscopy   ±   colonoscopy   with   a   view  to  confirming  the  cause  of  bleeding  and  endoscopic   treatment   (variceal   banding   or   glueing)  after  the  patient  has  been  resuscitated  and stabilised.

-        • If  bleeding  persists  and  oesophageal  varices  are   suspected   or   known,   consider   inserting   Sengstaken–Blakemore  tube  if  available,  else  use the largest-sized Foley catheter into stomach and inflate balloon (as per packet).

-        Apply gentle traction until there is resistance (so that balloon abuts  gastro-oesophageal  junction,  compressing  feeder vessels to oesophageal varices).

-        Take care not  to  exert  excessive  traction  thereby  pulling  balloon  into  oesophagus.  This  may  dislodge  clot  or  rupture  the  oesophagus.  Usually  this  is  rarely required and variceal banding and glueing is undertaken

Ascites à

-        The  production  of  ascites  is  complex  and  related  to portal hypertension.

-        Most children with chronic liver  disease  and  ALF  will  present  with  ascites,  although it is rare as an acute presentation of ALF.

Management è

-        Thorough   clinical   examination     or     ultrasound     if     unsure.    

-        Ultrasound  -  distinguish  ascites  from   intraperitoneal   blood   loss.  

-        Rapid   development  of  increasing  ascites  may  indicate  spontaneous bacterial peritonitis (SBP).

-        Specific management is required only if affecting feeding or ventilation

-        Use diuretics (spironolactone, frusemide).

-        • Maintain  albumin  in  the  normal  range  with  infusion of 20% albumin, giving a single dose of frusemide 1 mg/kg midway or at end of infusion.

-        • If      there      is      respiratory      compromise,      consider  peritoneal  tap  and  replace  with  IV  albumin 5 g/1000 mL of fluid removed.

-        Send a sample of the ascitic fluid for microscopy, culture,  cell  count  and  albumin  for  surveillance  of SBP.

Bacterial Peritonitis è

-        Common   and   severe   complication   of   cirrhotic   patients   with   ascites. 

-        Common   organisms  include  E.  coli,  Streptococcus  viridans,  Staphylococcus  aureus  and  Enterococcus  fecalis.

-        Clinical presentation - fever,    leucocytosis,    shock,    abdominal    pain/tenderness or only increasing ascites.

Management à

-        Peritoneal    tap    for    microscopy,   culture   and   cell   counts.  

-        Blood   cultures must also be obtained and sepsis workup should   be   included.  

-        Peritoneal   tap   findings   having   more   than   250   polymorphonuclear   cells/mL  are  suggestive  of  infection  (calculate  ratio for WBC to RBC if peritoneal tap is blood stained).

-        • IV   antibiotics   empirically   must   be   started.  

-        Choice  usually  is  cefotaxime,  and  changed based on cultures.

-        20% albumin IV may be needed at diagnosis following  tap. 

-        Antibiotics  are  continued  for  at  least 5 days.

Haemodynamics and Fluid Status in ALF è

-        • Hypovolaemia  and  dehydration  are  important  causes of precipitation of encephalopathy.

-        • Low  systemic  venous  return  (SVR)  in  ALF  leads  to  frequent  hypotension  and  bounding  peripheral pulses.

-        • If in shock, correct haemodynamics with one or two isotonic fluid boluses, and start vasopressors/inotropes  early. 

-        Dopamine,  noradrenaline  and  adrenaline are useful.

-        • Avoid  vasopressin  in  ALF;  it  is  associated  with  increase  in  cerebral  blood  flow  and  worsening  I C P.

-        • Children  in  ALF  are  more  prone  for  secondary  hyperaldosteronism  and  so  if  they  are  not  in  shock  then  it  is  preferable  to  start  the  child  on  two-third  maintenance  fluid  (isotonic  dextrose  containing  fluids). 

-        Beware:  Blood  products  are  a  common  cause  of  fluid  overload. 

-        Maintain  negative fluid balance yet euvolaemia.

-        Maintenance  of  high  normal  serum  sodium  (140–150  mEq/L)  helps  in  decreasing  cerebral  oedema. 

-        If  serum  sodium  is  persistently  <140  mEq/L, restrict fluids further.

Renal Insufficiency in ALF è

-        • Renal  failure  is  a  marker  of  poor  prognosis  in  ALF.

-        • Renal insufficiency in ALF can be due to various reasons:

–Dehydration and pre-renal failure

–Acute tubular necrosis

–Hepatorenal syndrome

-        • Diuretics can precipitate hepatic encephalopathy by causing hypovolaemia.

-        • Avoid nephrotoxic drugs and drug dosing has to be modified accordingly.

-        • CRRT  is  the  best  modality  of  renal  support  in    ALF    as    it    helps    to    prevent    sudden    haemodynamic    changes    causing    improved    stability   of   cardiovascular   and   intracranial   parameters. 

-        Peritoneal  dialysis  can  be  used  in  smaller children and infants.

-        Common  metabolic  derangements  seen  in  ALF  include  hypoglycaemia,  acidosis  or  alkalosis,  hypokalemia,  hypophosphataemia,  hypomagnesaemia,  low  ionised  calcium  and  poor    nutrition.

-        Nutritional  goals  of  a  patient  with  ALF: 

(i)             calories,  100–120  kcal/kg/day;  and 

(ii)          Proteins,  1–1.5  g/kg/day.  Role  of  branched  chain  amino  acids (BCAA) is not clear.

-        • The  best  way  to  provide  nutrition  in  ALF  is  enterally.

-        If oral intake is not possible then only TPN  can  be  started. 

-        It  is  preferable  to  convert  parenteral nutrition to enteral as early as possible as there is a high risk of infections with TPN.

Liver Support Systems è

-        –Plasmapheresis/double volume exchange

-        –Liver assist device: Non–cell based (artificial)

Haemoperfusion

Molecular  adsorbent  regenerating  system  (MARS)

-        –Liver assist device: Cell based (bioartificial)

HepatAssist: Porcine

ELAD: Human hepatoblastoma cells

Bioartificial   liver   (BAL):   Cryopreserved   human hepatocytes

-        –Auxiliary LT

-        –Hepatocyte transplant

Liver Transplantation è

-        Most  commonly  used  criteria  to  predict poor outcome and need for LT are King’s College  Criteria.

-        survival  ranges  from  70%  to  80%.

-        • Listing   of   patient:   The   decision   to   list   the   patient   must   be   made   when   the   likelihood   of  spontaneous  recovery  is  low  and  the  child  has  not  suffered  irreversible  cerebral  injury  or  respiratory failure.

King’s college criteria for liver transplantation è

-        Mitochondrial  disorders  and  haemophagocytic  lymphohistiocytosis   (HLH)   will   usually   not   benefit  from  LT. 

-        Ischaemic  hepatitis  usually  has  spontaneous  recovery  and  should  not  be  considered for LT.

-        Relative   and   absolute   contraindications   to   transplantation  include  uncontrolled  infection  or  sepsis,  coma  with  irreversible  brain  injury,  active   or   recent   malignancy,   uncontrolled   intracranial  hypertension  or  severe  intracranial  haemorrhage   and   progressive   or   end-stage   extrahepatic disease or systemic disease that will not  be  corrected  by  LT.  Inadequate  cardiac  or  pulmonary function of a transplant candidate is a relative contraindication to major surgery.

-        • In view of the organ shortage, apart from whole LT,  split  LT,  grafts  from  living  donors  and  extended  criteria  donors  are  being  used

Miscellaneous points è

-        Causes of a Raised ALT and AST

-       

-       

-       

How will you insert this device?

Nepean ICU protocol for handling this device.

1.    Protect the airway.
Ideally, the patient should be intubated.
This prevents you from inserting the tube into the trachea accidentally, and prevents aspiration of pooling oesophageal blood or displaced gastric content.

2.    Inspect the tube and check the balloons for leaks.
LITFL also recommend to calculate the compliance of the balloon "by inflating the  balloon with incremental 100ml aliquots of air to maximal recommended volume (usually 250 -300ml for SBT, 450-500ml for Minnesota) and note the corresponding balloon pressure at each step". This is highly appealing to any person who enjoys graphs.

3.    Lubricate the tube.

4.    Position the patient sitting up to 45°
This protects them from aspiration

5.    Insert the tube into the mouth or nose.
The college answer offers the nares as an option, but realistically everybody always uses the orogastric route because these patients are always coagulopathic and thrombocytopenic from their chronic liver disease. Moreover, the tube is huge and thick, with big balloons- they will shred the nasal mucosa on the way in regardless of how much lube you cake them in. The insertion should ideally be performed under direct laryngoscopy so that you can be sure you are in the oesophagus.

6.    The tube should be advanced to 50cm. 
The college answer prescribes a depth of 50cm, which is consistent with the classical technique for insertion (Bauer et al, 1974). The alternative is to measure from mouth to angle of the jaw, then suprasternal notch and xiphisternum. LITFL authors recommend the latter method, acknowledging that humans vary in the length of their oesophagus. 

7.    Inflate the gastric balloon. Check position with a chest Xray.
There seems to be some disagreement as to how much one might inflate. The college recommend 250ml; LITFL mention that the Minnesota tube should take 450-500ml. Locally, we are more cautions: we inflate with about 100ml and then check position with an AXR. If one has produced a compliance curve for their balloon, one may check the balloon pressure against their curve to see whether it has been inflated in the oesophagus (LITFL offer a 15mmHg increase in pressure as a rough guide: if the post-insertion pressure for a given volume is more than 15mmHg higher than the pre-insertion pressure, then the balloon needs to be repositioned as it is likely in the oesophagus. )

8.    Withdraw the tube until resistance is felt (at 30-35cm)
This is usually the depth to the gastro-oesophageal junction. Tension develops, which gives one the impression that the balloon is up against an obstacle of some sort. If one has not inflated with enough air there will be no resistance, and the balloon will come out of the mouth to theembarrassment of the operator. 

9.    Aspirate the gastric and oesophageal ports.
If there was vigorous bleeding, it should have stopped by balloon tension.

10. Decide whether or not to inflate the oesophageal balloon.
If you already know where the varices are on the basis of a gastroscopy result, you may use your judgment (i.e. there is no point of inflating the oesophageal balloon for gastric varices). Otherwise, one is guided by blood loss.  If bleeding from oesophageal and gastric ports has ceased,  then you may leave oesophageal balloon deflated. Bauer et al (1974) recommend to irrigate the suction ports with warm saline, to assure oneself that the aspirate returns clear and that there is no new bleeding.

11. If appropriate, inflate the oesophageal balloon to 25-30 mmHg pressure.
The maximum oesophageal pressure is 40mmHg. If the bleeding in the oesophagus has stopped, one should deflate the oesophageal balloon by 10mmHg every 2 hours.

12. Apply traction to the tubing
The precise amount of traction is uncertain. Some centres specify 1kg, others 2kg. The college answer calls for a 500ml bag of fluid, suspended over a pulley.

-        Link to join DTaP PICU Group è https://t.me/+in4hkN3oWCUxMmY1

-        Link to join DTa Ppedia à https://t.me/+C17Q8ftUCrM2Y2Rl

STATION 10

A previously healthy 6 year old female came with C/O fever for 2wk, and difficulty in breathing for last 3 days, on admission pt had tachycardia, tachypnoea with feeble femoral pulses and 2-D Echo show Dilated left ventricle with Ejection fraction <15%, BP in Upper limb was 134/96 while in Lower limb 72/54. A diagnostic imaging modality was done shown below in figure. Look at the figure and answer the following?

Marks

Q 1)     What is this diagnostic imaging modality ?                                                               1

Q 2)     What is the arrow showing in above depicted picture?                                       1

Q 3)     Identify the diagnosis ?                                                                                                      1

Q 4)     Write any two differential diagnosis of above condition ?                    0.5*2=1

Q 5)     Write any one management option.                                                                             1

Pathophysiology of dialysis disequilibrium syndrome

At a basic level this is a condition which results from the cerebral oedema that occurs when an ineffective osmole is enthusiastically extracted from the extracellular fluid by dialysis. In this, it resembles the cerebral oedema that can develop with the rapid overcorrection of glucose in a patient with a hyperosmolar hyperglycaemic state.  Its one of those rare disease states that, when first recognised, was immediately and fully understood by the authors of the seminal article, with little else added in the subsequent years.

That seminal paper was Kennedy et al (1962), and is really just a letter to the editor of the Lancet. This group of clinicians noted that among renal failure patients with uraemia, a group failed to improve following dialysis - instead developing worsening confusion even while their biochemistry looked better. They made the connection between this phenomenon and the urea concentration, taking a hint from contemporary neurosurgical practices (where at the time it was routine to give doses of urea for cerebral oedema, in the same way as in the modern era one might give mannitol). Coming to the conclusion that some sort of a reverse version of this effect must have been operating in their patients, they followed this up with a series of experiments, demonstrating the lag between blood urea and CSF urea concentrations. In this manner, Kennedy et al were able to demonstrate that a concentration gradient is established during and after dialysis.

Cold Shock: Dopamine / Adrenaline first-line. Warm Shock: Noradrenaline first-line.

PALICC-2 Criteria: Oxygenation Index (OI) = (MAP x FiO2 x 100) / PaO2.