anaesthetic consideration for lieno renal shunt surgeries

1. Portal hypertension and anesthetic
concerns for lienorenal shunt
surgery (HRS,HPS,PPHT)
Speaker: Dr.Vamshidhar
Dr. Rabbani
Moderator: Dr. Gopinath sir

2. OBJECTIVES
1. Anatomy of portal vein
2. Portal hypertension –definition, causes
3. Consequences
4. Management of acute varices
5. Hepatorenal syndrome
6. Hepato pulmonary syndrome
7. Portopulmonary hypertension
8. Anaesthetic management

3. ANATOMY
Portal vein is formed by superior mesenteric and splenic vein.
It is located in front of IVC and behind the neck of the pancreas at the level of 2nd
lumbar vertebra.
It is 7-8 cm in length & contains no valves.
Responsible for 70% total hepatic blood flow & 50-60 % o2 supply (o2 sat.: 60 – 75
%)

4. Normal Portal Pressure: 5 mmHg,
Portal Blood flow: 1-1.2lit/min
PORTAL HYPERTENSION is an increase in pressure gradient between
portal vein & hepatic veins or IVC
As the portal venous system lacks valves, resistance at any level between
right side of the heart & splanchnic vessels result in retrograde
transmission of an elevated pressure.

5. MEASUREMENT OF PORTAL
VENOUS PRESSURE
The portal vein pressure is a product of the portal blood flow volume and
the resistance to flow as defined by an application of Ohm’s law
Pressure = Blood flow * Resistance
Because of its invasive nature, the direct measurement of the portal
pressure is not routine.
As a less invasive and indirect measure, the hepatic venous pressure
gradient (HVPG) is considered the best surrogate indicator of portal
hypertension in cirrhosis
HVPG can be calculated by the subtraction of the wedged hepatic vein
pressure (WHVP) from the free hepatic vein pressure (FHVP)
HVPG = WHVP - FHVP

6. CAUSES OF PORTAL HYPERTENSION

7. increased resistance to
hepatic blood flow due
to cirrhosis and
regenerative nodules
PORTAL
HYPERTENSION
The increased
splanchnic blood flow
due to splanchnic
vasodilation

8. Major Consequences
Ascites
Portosystemic venous shunts and varices.
Congestive splenomegaly & hypersplenism.
Hepatic encephalopathy.

9. NORMAL
PORTAL
HYPERTENSION
CLINICALLY
SIGNIFICANT
VARICEAL
BLEEDING AND
ASCITES
1-5 mm Hg ≥ 6 mm Hg ≥ 1O mm Hg ≥ 12 mm Hg

10. Complications of Liver Cirrhosis
Liver
Cirrhosis
Liver
Insufficiency
Variceal hemorrhage
Portal
Hypertension
Ascites
Encephalopathy
Spontaneous
bacterial
peritonitis
Hepato-renal
syndrome
Jaundice

12. DIAGNOSIS
• mostly clinical.
• ULTRASOUND: on duplex ultrasound visualisation of cavernous transformation
of portal vein.
• ABDOMINAL CT: portal vein thrombosis,
portal vein dilation

13. • Indirect indicators like presence collateral pathways showed as obliterated
umbilical vein, located in the round ligament of liver and veins in the
phrenicocolic ligament, the gastric fundus or abdominal wall
• ascites, splenomegaly
• TRANSIENT ELASTOGRAPHY: hepatic fibrosis.
• ESOPHAGOGASTRODUODENOSCOPY: helps in assessment and
treatment of varices

14. VARICEAL BLEEDING
• Variceal hemorrhage most common complication
• 90% with cirrhosis develop varices.
• 30% of these bleed.
• The first episode is estimated to carry a mortality of 30%.
Sites for PORTOSYSYTEMIC SHUNTING
SITE PORTAL
COMPONENT
SYSTEMIC
COMPONENT
CLINICAL
EFFECT
LOWER
ESOPHAGUS
Lt. gastric vein Azygous vein GE varices
UPPER ANAL
CANAL
Sup. Rectal vein Inf. & Middle rectal
veins
Hemorrhoids
UMBILICAL Ligamentum teres
veins
Sup/Inf epigastric
veins
Caput medusae
RETRO-
PERITONEAL
Colonic veins Body wall veins

15. Management of Varices
Primary Prophylaxis: to high risk of bleeding /hematemesis
1. Non cardioselective  blockers -  portal & collateral blood flow,  in cardiac
output & Splanchnic vasoconstriction
Dose: Propanlol - 40mg 2-3 times/day
Nadolol – half of propanlol OD.
2. Vasodilators-  portal & collateral blood flow & variceal pressure
Isosorbide mononitrate (ISMN) is given when blockers are contraindicated.
Tolerance is common on long term therapy.

16. Role of Anaesthesiologist
 Procedure done  oropharyngeal LA in adults.
 Aspiration prophylaxis.
 IV with large bore needle.
Blood Cross matched.
 Monitoring.
 Children endotracheal anaesthesia.
 Extubate awake.

17. Management Of Acute Hematemesis
•Protection of airway if sensorium is altered and airway protective
reflexes are compromised
•Breathing: assisted ventilation if needed
•Circulation:
RESUSCITATION:
• i.v. access should be established with two wide bore 16 G cannulae
and a blood sample immediately obtained
• The patient should also be cross-matched for six units of blood.
• Volume replacement can initially be with either a crystalloid (e.g.
isotonic saline) or a colloid

18. • If the patient is haemodynamically stable with no evidence of
ongoing bleeding it is reasonable to wait for the haemoglobin
result before instituting blood transfusion.
ANTIBIOTICS
Gram-negative bacteria have been most commonly isolated in these
patients; therefore, antibiotics such as ciprofloxacin are appropriate.

19. Pharmacological management
i)Octreotide(somatostatin analogue) -  splanchnic blood flow & portal venous pr.
Dose: Octreotide - 250 µg I.V. bolus, followed by infusion 25 to 50 µg/hr for 2 to
4 days
ii)Vasopressin: a strong splanchnic vasoconstrictor, dose- 20 U I.V. bolus over 20
minutes, followed by infusion of 0.2 to 0.4 U/min, watch for myocard. ischaemia
NTG, initial rate of 50 µg/min (titrated to BP tolerance) effectively  cardiac
complications of vasopressin
iii)Terlipressin:long-acting vasopressin analogue 2mg as IV  by 1 or 2mg every 4
to 6 hrs

20. Endoscopic Therapy
• The endoscopic techniques used to achieve haemostasis by either interrupting the
collateral blood flow by immediate occlusion, such as with band ligation or tissue
glue, or by causing thrombosis with sclerotherapy.
• SCLEROTHERAPY:
• 1 to 5 mL of sclerosant is injected at each site (total Volume 10- 15ml)
• 5% sodium morrhuate, 1% to 3% Na tetradecyl sulfate, & 5% ethanolamine oleate
• Injected during active variceal bleeding.
•  Frequency & severity of recurrent esophageal variceal bleeding .
• Repeated at 7 to 14 day intervals until obliteration of varices occur.
• BANDING: placement of rubber O-rings on variceal columns
• Hemostasis achieved by physical constriction of varix at or near bleeding site

21. Sclerotherapy
Complications
•Injection induced bleeding
•Postinjection ulceration & delayed bleeding
•Postinjection ulceration esophageal ulcers
•Esophageal perforation (0-6%)
•Respiratory complications (0-6%)
•Sepsis (0-7%), chest pain (25-50%), fever
•Pleural effusion (16-48%), Mediastinitis
•Esophageal stricture (3-59%), Dysphagia
• Pulmonary Embolism: sclerosant in azygos vein

22. GLUE :
 Cyanoacrylate glue is injected into the varices and has been found to achieve
haemostasis in nearly 100% of cases.
 Re-bleeding rates have been documented to be as low as 2%.
BALLOON TAMPONADE :
 A Sengstaken Blakemore tube is effective in controlling variceal bleeding in
approximately 90% of cases.
 It has two balloons and one aspiration ports (gastric) and can be passed orally or
nasally.
 Gastric balloon is inflated with with approximately 200 ml of air will achieve
haemostasis.
 If bleeding persists, the oesophageal balloon should also be inflated.
 The oesophageal balloon should be deflated and re-inflated every 12 h to prevent
oesophageal necrosis

23. 40 to 50 ml of air
initially x ray 
Max. 300 ml of air
hemorrhage not
controlled 
esophageal
balloon is
inflated to 35 to
40 mm Hg.
Suction drainage
is applied to both
port

24. Minnesota balloon for tamponade
Bleeding Contd. Endoscopic therapy
Transjugular intrahepatic portosystemic shunt

25. TIPS
 Transjugular intrahepatic porto-systemic shunt
 Uncontrolled variceal bleeding following failed medical therapy & endoscopy
 Performed via IJV  LA with sedation
 Hepatic vein is cannulated with needle under USG & fluoroscopy guidance
 Tract created through liver parenchyma from hepatic to portal vein
 Tract is dilated & an expandable metal stent inserted to create Intrahepatic
Portosystemic Shunt
 Success rate is high with lower procedural morbidity & mortality
Bleeding, encephalopathy in 25%, & 50% of shunts may
occlude by 1st year

27. BLEEDING RELATED
COMPLICATIONS
Vascular collapse, hypotension
Encephalopathy
Aspiration
COMPLICATIONS OF THE
THEREPEUTIC PROCEDURES
Rebleeding
Oesophageal ulceration
Sub acute bacterial
peritonitis
Oesophageal perforation
Pulmonary aspiration
COMPLICATIONS OF VARICEAL BLEEDING

28. Surgical Procedures
Aim: To control portal hypertension & prevent recurrent
variceal bleeding
a) Portosystemic shunt procedures
b) Esophagogastric devascularization
c) Orthotopic liver transplantation
Selectiv
e shunts
Nonsele
ctive
shunts
PORTOSYSTEM
IC SHUNT
PROCEDURES

29. Nonselective portosystemic shunts
Immediately or eventually divert all portal blood flow from liver
into systemic venous circulation
1. End-to-side portocaval shunt
2. Side-to-side portocaval shunt
3. Interposition shunt: portacaval, mesocaval, mesorenal &
proximal splenorenal shunt
Complications: Hepatic encephalopathy, Bleeding, Shunt
thrombosis

30. End to Side Side to Side
Portocaval
Shunt
Prox. Splenorenal Shunt
Interpositional Shunt
1-Portocaval
2-Mesocaval
3- Mesorenal

31. Selective portosystemic shunt
 Selectively decompresses esophagogastric veins while
maintaining hepatopedal flow from mesenteric veins.
 Anastomosing distal splenic vein to left renal vein & interrupting
venous collaterals.
 Contraindicated in refractory ascites, splenic vein thrombosis,
previous splenectomy & small (< 7 mm) splenic vein.
 Complications: Bleeding, Ascites formation, hepatic
encephalopathy

33. ASCITES
Ascites is pathological accumulation of fluid in the abdominal cavity.
FACTORS RESPONSIBLE FOR DEVELOPMENT OF ASCITES
i) Decreased synthetic function of liver HYPOALBUMINEMIA
decreased oncotic pressure leaking of fluid in abdominal cavity.
ii) NO induced activation of RENIN ANGIOTENSIN ALDOSTERONE SYSTEM
SODIUM & WATER RETENTION.
iii)Raised intrahepatic vascular resistance along with with splanchnic vasodilatation
increases portal flow.
iv)Increased lymph production & seepage from disrupted lymphatic channels.

35. EFFECTS OF ASCITES
 Distended abdomen  intra abdominal pressure  protrusion of
hernias.
 Elevation of diaphragm & splinting of lower ribs.
 Accumulation fluid in Rt. Pleural cavity contribute to respiratory
embarrassment.
Edema feet.
 Increased incidence of Spont. Bacterial peritonitis – ascites becomes
infected in absence of recognizable cause of peritonitis.should be
differentiated from sec. bact. Peritonitis.
 PMN > 250 cells/ul is GOLD STD. for dignosis.

36. Ascites: Treatment
1. Rest, Salt restricted diet 1.6 – 2.0 gms/day
2. Diuretics: Spironalactone 100-400 mg/day
3. Frusemide: 40mg/day
4. Complications of diuretic therapy: Hypokalaemia, ppt of hepatic encephalopathy,
hypochloraemic acidosis, muscle cramps, rising BUN & creatinine
5. Therapeutic abdominal paracentesis: 5 lit safely removed
6. 5-10 lit removal replaced by salt free albumin 6-8 gm/lit fluid removed

37. Refractory Ascites
DEFINITION:
Ascites unresponsive to 400 mg of spiranolactone or 30mg of
amiloride plus 120mg frusemide daily for 2 weeks
Treatment:
TIPS
Peritoneo Venous Shunt( LeVeen Shunt ) designed for Spontaneous
unidirectional flow of ascitic fluid in supine position abdomen to vascular
system
 previous abdominal surgery,spontaneous bacterial peritonitis & large varices
are RELATIVE CONTRAINDICATIONS for shunt.

38. Hepatopulmonary Syndrome
Definition: Triad of-
1. Liver dysfunction
2. Intrapulmonary vascular dilatations (IPVD) in absence of detectable primary
cardiopulmonary disease
3. Hypoxaemia on breathing room air
Clinically: No symptoms, clubbing, cyanosis, Platypnea (dyspnea on sitting up),
Orthodeoxia (hypoxemia worsens on sitting up & improves on lying flat)
Pathophysiology: Widespread IPVD mainly in bases of lung with resultant  AV
shunting

39. Hepatopulmonary Syndrome
Diagnosis:
1. Echocardiogram- + ve bubble study (appear in Left Atrium with in< 7 beats)
2. ABG on room air & 100% O2 (A-a gradient>15 mmHg)
3. IV technetium-99m–labeled albumin transit the lungs, appear in kidney and brain
4. Pulmonary Angiography- diffusely fine or blotchy vascular configuration
Treatment: O2, Somatostatin to inhibit vasodilation, coil embolization, Inhaled NO ,
Liver Transplant reverses partly

40. Hepatorenal syndrome
DEFINITION:
This is a discrete entity which is essentially a diagnosis of exclusion in
cirrhotic patients. It is defined as the occurrence of renal failure in a
patient with cirrhosis in the absence of another identifiable cause..
It is characterized by azotemia, hyperosmolar urine, and urinary sodium
excretion less than 10 mEq/L

41. Diagnosis

42. Subtypes
Type 1: cirrhosis and rapidly progressive RF. It causes doubling of
creatinine in less than 2 weeks. It may arise spontaneously or in
association with treated spontaneous bacterial peritonitis
Type 2: Cirrhosis and subacute RF. This type is characterised by stepwise
deterioration of renal function over a longer time period.
The median survival is longer than in type 1 HRS
Type 3: cirrhosis with types 1 or 2 HRS superimposed on chronic renal or
acute kidney injury.
Type 4: Fulminant liver failure with HRS

44. Treatment
1.Volume restoration
Discontinuation of diuretics and volume expansion with albumin at 1g/kg (5ml
20%/kg), followed by 20-40g/day
2.Systemic vasoconstriction
Terlipressin is a powerful Vasopressin V1 receptor agonist which causes systemic
vasoconstriction and raises blood pressure.
It is long – acting and generally commenced at a dose of 1 mg QID iv, increasing to
a maximum of 2 mg 4-hourly .
Octreotide, a somatostatin analogue, can be substituted if there is known coronary
disease or other ischaemic contraindication.

45. 3.Renal replacement therapy
•Patients with type 1 and type 4 HRS with established multi- organ failure are given
renal replacement therapy (RRT).
•RRT does not improve prognosis but helps to ameliorate fluid overload, acidosis and
hyperkalaemia.
4.TIPSS
It can lower portal pressure and prevent splanchnic pooling.
Many patients with type 1 HRS are too ill to undergo TIPSS and it carries significant
complications; notably worsening hepatic failure, cardiac overload due to increased
venous return, and encephalopathy.
Extracorporeal therapies
Extracorporeal therapies such as the molecular adsorbent recirculation system (MARS)
have been shown to reduce ammonia, bilirubin and creatinine levels.
Currently, similar to TIPSS, it is primarily a bridging tool to transplant.

46. Orthotopic liver transplant (OLT)
Patients with type 1 and 4 HRF should be evaluated for OLT.
Patients with type 3 HRS or chronic ATN together with HRS may require
combined liver and renal transplantation.
After successful OLT results in resolution of HRS in the transplanted patient,
one third of these patients require renal support post-op.
On-going renal impairment post transplant may require dose reduction of
anti-rejection immunosuppressants such as cyclosporin or tacrolimus.

47. Portopulmonary hypertension
PPHTN is considered to be present when PAH exists in a patient who has coexisting
portal hypertension, and no alternative cause of the PAH exists
PATHOGENESIS
●Imbalance of vasoconstrictive and vasodilatory mediators :
The most widely accepted hypothesis
Humoral substances which would normally be metabolized by the liver is able to
reach the pulmonary circulation through portosystemic collaterals, resulting in
PPHTN.
serotonin, interleukin-1, endothelin-1, glucagon, secretin, thromboxane B2, and
vasoactive intestinal peptide.
● Genetic predisposition
● Thromboembolism from the portal venous system

48. CLINICAL PRESENTATION
symptoms and signs suggestive of PAH (eg, dyspnea on exertion, atypical chest
pain, elevated jugular venous pressure, leg edema)
●Elevated mean pulmonary artery pressure (mPAP) >20 mmHg at rest
●Normal or low pulmonary capillary wedge pressure ≤15 mmHg at rest
●An elevated pulmonary vascular resistance [240 dynes/sec/cm]
The interval between the first manifestation of portal hypertension and the
documentation of PAH ranges from 2 to 15 years
TREATMENT: should be treated with general measures which target portal
hypertension as well as the complications of pulmonary arterial hypertension
 Phosphodiesterase-5 inhibitors (PDE5Is) like sildenafil and tadalafil are
commonly prescribed since their metabolism is not affected by liver dysfunction
 Prostacyclin pathway agonists : Epoprostenol ,Treprostinil
 Avoidance of beta-blockade , anti coagulants.

49. Managing Coagulation Defects
Vit K1, 10mg, IV for 3days
FFP: good source of clotting factors
Fresh blood : factor V & platelets in addition to VII,VIII & X ( in stored blood)
Platelet rich plasma concentrate
Recombinant factor VIIa: 40-80µgm/kg ( corrects PT)
Desmopressin: vasopressin analogue-  in factor VIII & von willebrand
factor:  bleeding time & PTT
 Dose 0.3mg/kg, repeat if required 8 hrs later

50. Anaemia :
Causes
Blood loss from varices
Nutritional deficiency (B12, folic acid)
Hypersplenism
Depressive effect of alcohol on bone marrow

51. HEPATIC ENCEPHALOPATHY
Hepatic encephalopathy is a potentially-reversible neuropsychiatric abnormality
that complicates liver disease
Clinical presentation
•Disturbed consciousness-somnolent
•Personality changes- irritable
•Intellectual deterioration
•Speech – slow, slurred, monotonous
•Flapping tremors
•Fetor hepaticus- sour, fecal smell of breath
•Blood Ammonia level elevated
•EEG –slowing of all waves with increase in amplitude
•CT- may show cerebral edema

52. GRADING OF HE
GRADE STATUS
0 Alert & Oriented
1 Drowsy but oriented, able to talk, disordered sleep
rhythm
2 Drowsy and disoriented, altered mood
3 Agitated & Aggressive,unable to perform mental task,
confusion
4 Comatous, with/ without response to deep pain

53. Events precipitating hepatic encephalopathy
1. Electrolyte imbalance
2. Diuretics
3. Vomiting
4. Diarrhoea
5. Gastrointestinal bleeding & Gastroduodenal erosions
6. Drugs: Narcotics, benzodiazepines
7. Alcohol withdrawal
8. Infection-Spontaneous bacterial peritonitis.
9. Constipation
10. Dietary protein overload

54. Treatment
 Correction of precipitating factors, evaluate for G.I bleeding.
 Eliminate sedatives/tranquilizers.
 Reduce protein intake.
 Correction of hypokalemia- renal NH3 production which can cross blood-br.
barrier .
 Lactulose-affect ionization of ammonia in colon & facilitates its absorption in
colon.
 Antibiotics- to kill intestinal flora (Neomycin/metronidazole/vancomycin)
 Benzodiazepine receptor antagonists.
Flumezenil- induce transient improvement in neurological status
- L-ornithine-L-aspartate: stimulates urea cycle- reduces ammonia level
Provide supportive care with attention to airway, hemodynamic and metabolic
status.

55. Preoperative Assessment
History: causative agent, duration, effort tolerance, jaundice, hematemesis, ascites,
associated co morbid conditions, previous medications or surgeries
Clinical examination- signs of liver cell failure, through examination of respiratory
and cardiovascular system

56. Preoperative Investigations
Complete blood Count- Platelet count, anaemia, leukocytosis
Liver function tests.
S.Creatinine, Blood urea.
Blood Sugar
PT, INR, APTT
Xray Chest
ECG,ECHO cardiography
PFT,ABG

57. Preoperative Optimization
Correction of anaemia, thrombocytopenia
Hypoproteinemia correction- plasma / saltfree albumin
Correction of coagulation defects
Tense Ascites –Paracentesis
Drainage of pleural fluid
Antibiotic prophylaxis
Correction of electrolyte and acid base disturbances
Chest physiotherapy, breathing excercises

58. Monitoring
ECG, SpO2, EtCO2
Urine output
Temperature monitoring
GRBS
Invasive BP- ABG/ non invasive BP
CVP, pulmonary arterial catheter/ TEE

59. Anaesthetic drugs
Hypoalbuminemia impairs drug binding
Elevated serum drug levels
Decreased metabolism and excretion
Prolonged drug effects
Increased volume of distribution
Necessitates larger initial dose

60. Anaesthetic drugs
I.V induction agents (titrated doses)
Thiopentone, propofol
NM blockers (initial larger dose, prolonged effect)
Atracurium, cisatracurium- hoffman elimination –safely used.
Concerns regarding Laudanosine (hepatic clearance-seizure)
Pancuronium & vecuronium are highly protein bound-prolonged action.
Rocuronium increased initial dose & prolonged action

61. OPIOIDS
Morphine/Pethdine- metabolised in liver to active form-prolonged action
Fentanyl & Remifentanil can be used
INHALATION AGENTS
Isoflurane, Sevoflurane,Desflurane can be used safely- do not decrease hepatic
blood flow
Haothane- max. decrease hepatic blood flow
halothane hepatitis
type I-benign,self -limiting
type II-immune mediated fulminant
liver cell failure because of trifluroacetyl metabolites

62. Anaesthesia Technique
1. Premedication: antisialogogues.
2. Preoxygenation
3. Induction: Thiopentone / Propofol
4. Ketamine may be used if hemodynamic instability
5. Rapid sequence intubation with Suxamethonium
6. Controlled Ventilation With atracurium, Air+ O2+ Isoflurane/
Desflurane
7. Analgesia: Fentanyl /remifentanil
8. Avoid hypo/hypercarbia
9. Avoid lactate solutions

63. Intra-operative management
Maintain blood pressure
Avoid hypoglycemia
Avoid unnecessary oesophageal instrumentation
 gastric tube
Administer calcium after blood transfusion

64. Intra-operative problems
•Hemorrhage- b/o coagulopathy, hypothermia,- replace blood, FFP,
platelets & cryoprecipitate.
•Hypothermia-warming blankets, infusion of warm fluids
•Decreased urine output- diuretics, mannitol
•Hypotension
Causes of hypotension
-Blood loss -Traction on abdominal viscera
-Impaired catecholamine response -Sympathetic blockade
-Coagulation abnormality due to anaesthetics

65. Post operative Management
Pain relief: PCA morphine/ fentanyl
Regional block may be given if INR 1.5
Watch for hepatorenal syndrome, DIC, hepatic encephalopathy
 Avoid IM injections, continue antibiotics
Prophylactic ventilation till all parameters are acceptable
Diagnosis of DIC
Marked prolongation of PT
Fibrinogen < 1.0gm/lit
FDP > 100µgm/lit
Platelets< 10,000/mm3

66. Regional Anaesthesia
INR atleast 1.5
Dose of LA reduced
Spinal & epidural block can  hepatic blood flow(T4 level-  flow by 20%)
Possibilty of precipitus ciculatory collapse as hemodynamic responses 
 Sometimes epidural varices present can bleed– risk of hematoma 
 Possibility of Risk of infection

67. Anaesthetic concerns of spleno
renal shunt
PREOP CONCERNS
Poor preoperative nutritional status and anemia may lead to delayed wound
healing, delayed ambulation, and respiratory complications and infections.
Hypersplenism: thrombocytopenia, need for splenectomy
Variceal bleed: Patient will be on propranolol, repeated endoscopy for
sclerotherpy/banding,TEE
Ascitis: need RSI, Paracentasis induced cardiac dysfunction (PICD).
Pleural effusion: need tapping just prior surgery.

68. Porto-pulmonary HTN,Hepatopulmonary syndrome.
Hepato renal syndrome
It is recommended that thrombophilia be ruled out in cases of
EHPVO and anticoagulation. therapy should be started early in the
prothrombotic state especially to maintain the patency of shunt.
Cardiomyopathy

70.  INTRA OP CONCERNS
 Growth retardation, decrease lean body mass and loss of muscle
that may lead to postoperative respiratory failure
 Two large bore peripheral IV cannula preferably upper limb
Central line:
 As it's a vascular surgery plan for Massive transfusion & cell
salvage.
 Fluid warming device- Hot line.
 Splanchnic vasoconstriction and thrombosis leading to intestinal
ischemia must be avoided with adequate cardiac output, oxygen
delivery and decreasing release of stress hormones.

71. Degree of hepatic dysfunction: drug dosing, type of shunt (no Rex
shunt if cirrhosis)
careful when inserting Ryle's tube in view of varices, risk of
bleeding
Encephalopathy: careful when premedicating
Caution during epidural catheter placement weighing the
possibility of epidural space bleed due to low platelet counts,
anticoagulant therapy.

72. POSTOPERATIVE ISSUES:
 Upper abdominal surgery with severe pain may compound the problem of
pulmonary atelectasis.
 Shunt thrombosis: need anticoagulation.
 Post shunt/Portosystemic encephalopathy.
 Post splenectomy sepsis
 Increased cardiac output.
 Significant abdominal bleeding necessitates emergent reoperation.
 Chylous ascites: because of disruption of retroperitoneal lymphatic channels.
 Esophageal strictures after devascularization procedures and esophageal
transection are common.

74. REFERENCES:
1. Barash 5th edition
2. Harrison's Principles of Internal Medicine, 21e Eds. Joseph
Loscalzo, et al.
3. Approach to the diagnosis of portal hypertension Christopher Koh, M.D. and
Theo Heller, M.D.
4. Miller’s Anesthesia, 8th Edition. Anesthesiology 2016
5. Rebecca McKay, MBChB MRCP, Nigel R Webster, PhD MB ChB
FRCA FRCP FRCS, Variceal bleeding, Continuing Education in
Anaesthesia Critical Care & Pain, Volume 7, Issue 6, December
2007, Pages 191

75. PREVIOUS QUESTIONS
1.Pre anaesthestic evaluation and preparation of patient with portal
hypertension for lieno renal shunt.
2.Anaesthetic implications in patient with portal hypertension.
3.Hepato renal syndrome.