Call Girls Bareilly Just Call 9907093804 Top Class Call Girl Service Available
Obesity anaesthesia
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.
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
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
17.
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
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
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
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.
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
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%
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
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
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
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
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
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
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↑
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
Management of patients with obesity hypoventilation syndrome (OHS) from diagnosis to integrated care to modify health trajectories. After being diagnosed with OHS, these patients are typically initiated on positive airway pressure (PAP) therapy (continuous positive airway pressure or noninvasive ventilation). Although respiratory insufficiency improves quite consistently in patients adherent to PAP therapy, pulmonary hypertension may also improve in some patients with OHS. There is no evidence that other cardiovascular and metabolic comorbidities improve with PAP treatment alone. Therefore, a multimodality therapeutic approach is necessary to combine PAP therapy with strategies aimed at weight reduction and increased physical activity. PaCO2: arterial carbon dioxide tension.
Obesity hypoventilation syndrome (OHS) management strategy. Continuous positive airway pressure (CPAP) could be first-line treatment for OHS patients with concomitant severe obstructive sleep apnoea (OSA). Noninvasive ventilation (NIV) should be considered as first-line therapy for OHS patients with no OSA or milder forms of OSA. If patients initially treated with CPAP have no favourable response to therapy despite objectively documented high levels of adherence to CPAP, they should be changed to NIV therapy. AHI: apnoea–hypopnoea index.