morbid obese, resistant obesity, gastric by pass, poor respiratory reserves, pulmonary hypertension, ventilator essentials in obese patients

1. DEPARTMENT OF PULMONOLOGY
& CRITICAL CARE MEDICINE
SIMS/SHL
DR MUBASHAR SULTAN HASHMI
FELLOW CRITICAL CARE MEDICINE
DR M.OWAIS SIPRA
PGR PULMONOLOGY

2. CONTENTS
27 years old boy faisal muneer, resident of
mandi bahawudin, who had recurrent
admissions through emergency and needed
multiple interventions
We will discuss following details:
 Admissions.
Discussion of Clinical conditions and their
implication.

3. 1st Admission
 Referred to pulmonary department from
medical ward where he was admitted
through emergency on 10 January 2013 for
complaints of
 Dyspnea with fatigue 4 years
 Rapidly worsening dyspnea 2 weeks

4. He was in his usual state of health 4 years ago when
he started feeling shortness on breath that was gradual in
onset, Initially on heavy exercise and gradually
progressed to mild activity. Patient denied seasonal or
diurnal changes, chest pain or palpitation. He also denied
wheeze, sneezing, post nasal drip, orthopnea or edema of
feet.
2 weeks ago he had flu like illness with high grade,
continuous fever that lasted for 4-5 days followed by
cough. Cough was initially dry but became productive
with scanty white to yellow colored sputum and
associated with severe worsening of dyspnea that didn’t
improve with initial treatment and oral antibiotics by the
local GP( He can’t recall the names). He was referred to
Lahore due to severe dyspnea at rest and hypoxemia.

5.  His father reported that patient had disturbed sleep
with loud snoring that bothered his family
members. He used to Remain drowsy most of the time
of day and fall asleep even during work or watchingTV.
His somnolence got worse over time.
 He had normal bowel and bladder movements.
 Increased appetite without polyuria, or polydypsia, or
cold intolerance that led to marked weight gain.
 He could walk, climb stairs and never used sleeping
medicine or narcotics.

6. PAST HISTORY: His birth to childhood period was uneventful but
started eating more and putting on weight from the age of 12
years.
FAMILY HISTORY: Among five alive siblings one of younger sister
has 90 kg weight at the age of 10 year.
One brother and sister died at the age of 4 months and 2 years due
to cause family doesn’t know but they were normal physically.
PERSONAL HISTORY: Non- smoker, studied till class 4 and quit
due taunting behavior of his class fellows. Now working at mobile
repair shop.
SOCIOECONOMIC HISTORY: belongs to lower middle class
family. Father is a farmer and runs his grocery store.

7. EXAMINATION
Markedly obese male ,tachypnoic but oriented in time and space.
Pulse (regular) 110 B.P 120/70 Afabrile
R/R 35 O2 sat. 82% (room air)
Height 63 inch weight 195 kg
BMI 76 kg/sq. m
Central cyanosis +ve Thyroid not enlarged
Conjuctival hyperemia JVP not raised
Pedal edema -ve

8. SYSTEMICEXAMINATION
 Marked fat on the abdomen and chest wall
with abdomino-thoracic respiration.
 Respiratory, CVS, Abdominal, CNS examination
Were unremarkable.

9. LaboratoryWorkup
Hb% 18.0 Hct. 55
Random blood glucose 110 mg/dl
Arterial blood gases(Room Air):
PH: 7.37 PCO2: 48 PO2: 50 HCO3 27
O2 Sat (SO2) 82%
CXR & ECG- unremarkable
RFTs, LFT,TFTs, SE, Urine C/E ---Normal

10.  Spirometry was attempted but he was unable to
perform initially but after treatment his PFTs
showed
 FVC 60% of predicted
 FEVI 55% of predicted
 FEV1/FVC ratio 91%
 No significant reversibility after SABA
 Sleep studies: OSAS, AUTO CPAP TITRATION

11. Diagnosis
Morbid obesity
Obesity Hypoventilation
Obstructive Sleep Apnea Syndrome
Secondary Polycythemia

12. Management
Oxygen to keep O2 Sat >9O%
IV Antibiotics
CPAP with full face mask with 10 cm
Motivation to reduce weight
Early mobility

13. Discharged
Home CPAP Exercise
Non-
pharmacologic
plans of weight
reduction

14. Patient remained well and resumed the
work on his mobile shop

15. 2nd Admission
 Patient presented to pulmonary department with
acute onset worsening of dyspnea , no fever, no
productive cough or audible wheeze-- last 2 days
 Using CPAP regularly.
 He didn`t respond to oxygen and nebulization by local
GP.
 On presentation he was drowsy, severely hypoxic and
had pedal edema. Breath sounds were inappreciable
due to excessive fat.

16. Room Air O2 sat 70%.
Blood Gases:
PH: 7.30 PCO2 60
PO2 40 HCO3 30
X-Ray Chest: unremarkable
CBC, RFTs, LFTs and S/E : with in normal limits

18. Further Workup
ECG : sinus tachycardia
D-dimer : 3,000
Leg venous Doppler : Left leg DVT (popliteal/femoral)
CTPA: confirmed right inferior pulmonary artery PE
Echocardiography: RVH with PASP 45, no SWMA.

19. MANAGEMENT
DVT leading to
Pulmonary embolism
Hypoxic and hypercarbic
RF(Type-II)
Fondaparinux
VKA
Oxygen,
Nebulization
BIPAP in
hospital
settings

20. Discharged
Warfarin
with
PT/INR
monitoring
Home
CPAP

22. 3rd Admission(6monthslater)
 Increasing dyspnea, now dyspneic at rest.
 Swelling of legs and scrotum 4 weeks
 Bluish discoloration of finger and toes 3 weeks

23.  He had poor compliance towards the treatment
 Erratic dietary habits
 Poor compliance with CPAP usage.
 Remained bed ridden ate more food; gained
10 kg weight( total 205 Kg)

24. Examination
Morbid obesity with difficulty in breathing.
Vesicular breathing with prolong expiration, no
rhonchi or crepitation.
Scrotal, sacral and pedal edema was present.
Cardiac, abdominal, and neurological examination
was normal

25. Laboratoryworkup
Hb 18 Hct. 56
TLC 13000
Type -II Respiratory Failure on ABGs

26. ABGs
• pH 7.29
• PCO2 63
• HCO3 33
•PO2 40

27. Furtherworkup-----
NO DVT
No Pneumonia or Fluid Overload
USG ABDMOEN:
Fatty liver
Cholelithiasis without cholecystitis
Normal looking pancreas

28. FinalImpression
Poor compliance leading to:
massive gain in weight
worsening symptoms of OHS
secondary polycythemia &
cor-pulmonale/ pulmonary HTN

29. Management
 Antibiotics
 Furosemide with Aldactone
 BiPAP (IPAP 28, EPAP 08, Rate= 20)
 Nebulization
 Oxygen

33. SurgicalConsultation

35. Concerns:GS andAnesthesiateam
 Fitness for anesthesia was asked from
pulmonology department
 ECHO: good LV, moderate pulmonary
hypertension PAP 55, RVH
 SPIROMETERY:
FVC 40%, FEV1 35% FEV1/FVC 87

36. Normal flow pattern of left Common
femoral Artery & Vein:

37. Normal Flow pattern in left common femoral
Vein (with & without compression)

38. Normal Flow Pattern in the left
Popliteal Vein:

39. HRCT CHEST :
Subtle patchy ground glass haze on these Axial CT Images which
could be due to partial filling of air spaces during inspiration.

40. HRCT CHEST:
 Coronal Image: Subtle patches of ground glass opacifications .There is no
evidence of collapse, consolidation, bronchiectasis and fibrocystic
changes.

41. OUR RECOMMENDATION
HIGH RISK FORGA
PostoperativeICUCARE

42. Underwent Vertical Sleeve
Gastrectomy

43. X-RAY CHEST
Normal Pre op x ray. Normal post op x ray.

44. Post operative course in SICU
 Difficult to ventilate,Tachypneic
 Hypoxic on ventilator PCo2 increasing 80mmhg
 Fio2 100 spo2 80%
 VENTILATOR SETINGS:
SIMV/PS
TV 500 , PEEP 5, Rate 18 FIO2 100
Rate was increased to 26,, but PCO2
kept on increasing to 85mmHg

46. MEDICALICUCONSULTATION

47. Pulmo/critical care consultation
 Patients ventilator settings were readjusted
to help recruit the atelectasis lungs by
recruitment measures
 PEEP was gradually increased to 14,which
improved the oxygenation to spo2 100%

48. RECRUITMENT MANEUVEVORS

49. TransferredtomedicalICU

50. Post operativeCourse in the MICU
Ventilated for 3 days –Extubated and put on
NIPPV( BiPAP)
Developed abdominal pain
• raised serum amylase , lipase , transaminases and
Bilirubin
• mild pancreatitis
Managed conservatively, on CPAPAND
WARFARIN

51. DISCHARGED HOME

52. POST GASTRIC SLEEVE -2013
Marked weight loss
Weight reduced to 120 kg
CPAP AND OXYGEN FREE
STARTED PLAYING CRICKET EVEN

53. Continued……………….

54. FURTHER FOLLOW UP
 ANEMIA DUETO GI LOSSESS DUETO
UNMONITOREDWARFARIN
 AGAINWAS discharged home
 warfarin….
 Why Xeralto was not given…..Affordably
issue.

55. RE-ADMITTED
 Dyspnea and hypoxia, leg swelling
 Diagnosed as RECURRENT DVT with pulmonary embolism
 ON INQUIRY HE REVEALEDTHAT HE HAD STOPPED
WARFARIN DUETO FEAR OF GI BLEED
 Managed for PE and switched to NOAC- NON-VKA----
Rivaroxiban
 DISCHARGED HOME

56. 6 months Later………….

58. Admission
 Abdominal pain and vomiting
 Diagnosed as Cholecystitis & Biliary colic
 Upper Gi endoscopy: gastritis and hiatus hernia
 Managed conservatively
 Then was planned for cholecystectomy

59. CLINICAL ISSUES……
Morbid obesity REGAINEDWEIGHT; Benefits of
sleeve gastrectomy weaned off.
OSAS/ OHS: again became CPAP dependent,
worsening hypoxia, pulmonary hypertenion
Recurrent biliary symptoms
Recurrent pulmonary embolism and DVT

60. Anesthesia/ SURGERY: Risks???
Oxygen Dependent, spo2 80 % room air
CPAP upto 12 hours a day
Ongoing rivaroxaban
Weight 156 kg Body Mass Index=60
Deteriorating pulmonary functions:
FEV1= 40% FVC= 45% FEV1/FVC 88

61. What Else should be Done?????
Only cholecystectomy is
Enough???

63. BARIATRIC SURGERY
Laproscopic gastric bypass
and cholesystectomy

64. ANAESTHSIA CONCERNS
Anaesthesia was high risk,@ BMI 60, FEV1 , FVC
Long standing Pulmonary hypertension/cor
pulmonale
High risk consent - Table Death consent was
asked by the anesthesia
Risk vs Benefit was questioned by anesthesia

65.  Improvement in BMI/ morbid
obesity:
Prevent future events e.g DT/
PE.
Improvement in OSAS/OHS .
Pulmonary hypertension.
Improved QOL.

66. Faisalmadehismind
clear:
&
said:
“Hewillcommit
suicideifnotgot
operated”
MOTIVATION

67. Operation Day

68. Pre Op Assessment- in OR
Vitals: HR 90/MIN, 110/70, AFABRILE
Oxygenation: 88 % 3 L nasal cannula
Infromed and written Consent was secured
and father was counselled about the
anticipated worst possible outcomes , by the
anaesthesia consultant.

69. Pre op medication/optimization
 Oxygen
 Magnesium sulphate
 Fluid: 500 ml normal saline
 Inserted central venous line
 Started Milrinone preopertively before
induction
 Standby norepinephrine infusion

70. ANAESTHESIA
 Given by the Anaesthesia team
 Ketamine and MIDAZOLAM and inhalation
anaesthesia , Roucronium as a paralytic agent.
 Tracheal intubation
 Patient position: semirecumbent 35-40 degree
 Mutually agreed by the surgeon and anaesthesia
team-
 Ventilated :VC mode, PEEP 8-10, FIO2 titrable
 4 hours surgery/anaesthesia
 SEDATIONS: PRECEDEX / NELBUPHENE.

71. POST OPERATIVE
 Immediately transferred to MICU from the
OR
 Uneventful operation: laproscopic gastric
bypass and cholcyestectomy
 Uneventful recovery
 No hemodynamic unstability

72. ABGS AT START OF SURGERY ABGS @ END OF SURGERY

74. Post operative period: MICU
 Ventilated /sedated: high PEEP
 Weaning trial on 1st post op Day: not successful
 So we continued mechanical ventilation at High
PEEP 12-15 - Atelactasis/lung recruitment, with
judicious sedation
 Successfully weaned and Extubated on 2nd Post
Op Day. Post Extubation NIV

75. DISCHARGED HOME
No post operative compications
ON Discharge: 5 kg weight reduction in a week
time
Discharge on 26-08-2019 , 10 days after the
surgery
Home CPAP, OXYGEN AND RIVAROXABAN

76. Its not finished yet………….

77. DISCUSSION
 Morbid obesity
 Obstructive sleep apnea syndrome
 Pulmonary mechanics and obestiy
 Causes of obesity- leptin defciency
 Bariatric surgery- sleeve gastrectomy/ gastric
by pass
 Anaesthesia in morbid obese and pulmonary
hypertension

78. MORBID OBESITY

79. Obesity and ventilation

80. Lung physiology & Obesity
• Lung compliance↓
– Mass of adipose tissue compressing the chest
wall, the diaphragm and abdomen
– Stiffening of the total respiratory system
• Small airway resistance↑
– Functional residual capacity (FRC)↓
– Intrinsic airway narrowing
• Narrowing of the upper airway
– Compressing adipose tissue
– During sleep  OSA

81. Lung physiology & Obesity
• Static lung volumes↓ secondary to:
– Small airway closure
– Alveolar collapse
– TLC, FRC, ERV ,VC ↓exponentially with BMI↑

82. PathogenicMechanismOHS
90% have associated
OSA
High o2 consumption/ co2
production. Dec. ventilatory
drive

83. OBESITY HYPOVENTILATION SYNDROME
Obesity/BMI >30
Hypoxemia /sleep
Awake PaCO2 >45
Sleep Disordered Breathing: No other reason for
hypoventilation i.e, stroke, neuromuscular or endocrine disorder

84. Obstructive Apnea A blockage of the airway despite efforts to breath.
Notice the effort gradually increasing ending in airway opening.
Blood oxygen levels
reduce to < 4% of
baseline value
Inhale
Exhale Airway obstructs Airway opens
Paradoxing
Paradoxing Ends
EKG
Airflow
Thoracic
effort
Abd.
effort
SAO2
Effort gradually increases

85. Management of patients with obesity hypoventilation syndrome (OHS) from diagnosis to
integrated care to modify health trajectories.
Juan F. Masa et al. Eur Respir Rev 2019;28:180097
©2019 by European Respiratory Society
OXYGEN
THERAPY
CPAP: NOVEL
VOLUME
TARGETed
AUTO
BARIATRIC
SURGERY
MEDROXYPRO
GESTERONE
ACETAZOLAMIDE
Treatment of OHS

86. Obesity hypoventilation syndrome (OHS) management strategy.
Juan F. Masa et al. Eur Respir Rev 2019;28:180097
©2019 by European Respiratory Society
OSA NO OSA

87. Pulmonary Hypertension
intensivist/anaesthesia perspective

88. RECOMMENDATIONS
 VOLUME MANAGEMENT
 MONITOR FLUID STATUS CLOSLELY
 CAREFUL FLUID LOADING , MAYWORSEN RV
FUNCTIONS
 VASOPRESSORS

89. INOTROPES/ PRESSORS IN RV DYSFUNCTION
 Dobutamine
 Nor epinephrine
 Milrinone
 Levosimendan

90. Post op care: obese/PH
 Good pain control
 Avoid hyperthermia, hypertension
 Volume status/ cvp
 Rv support/ hemodynamic monitoring
 Awake ventilation/ psv, early weaning

91. Peri-operative care: Obese/ PH
 Avoid factors which increase PVR, Decrease Right
ventricular oxygen supply and increase the o2
demand .These are:
Hypoxia Hypecapnia Acidosis
Tachycardia Fluid overload
 The failing RV is very afterload sensitive, so
one of the key goals is to maintain pulmonary
arterial pressure (PAP) as low as possible to
maintain forward flow.

92. Ventilation in obese
 Position
 Sedation
 Lung protective strategy
 PEEP
 Extubation / NIV

94. LEPTIN DEFICIENCY

97. Sleeve Gastrectomy
 Resection of 80% greater
curvature
 Major reduciton in ghrelin
hormone which is a hunger
hormone
 55 % weight reduction

98. Gastric Bypass Roux-en-Y :Bariatric Procedure

99. IMPROVED LEPTIN RESISTANCE