1. Acute Pulmonary Edema During Emergence from Anesthesia Liu, Chih-Min 2003-9-22

2. History 51 y/o female 51 y/o female 68 kg 68 kg Past history: Past history: DM; HTN: noted > 2 years, under poor medical control DM; HTN: noted > 2 years, under poor medical control Clinical diagnosis: Vitreous hemorrhage, L ’ t side Clinical diagnosis: Vitreous hemorrhage, L ’ t side Operation: PPV on 2003-9-17 Operation: PPV on 2003-9-17

3. ASA class lll E BP: 237/134 mmHg at the OR BP: 237/134 mmHg at the OR Past history: Past history: DM; HTN: noted > 2 years, under poor medical control DM; HTN: noted > 2 years, under poor medical control

4. Induction Fentanyl 100 micro-gram Fentanyl 100 micro-gram Cis-atracurium 10 mg Cis-atracurium 10 mg Xylocaine 80 mg Xylocaine 80 mg Propofol 120 mg Propofol 120 mg Esmolol 25 mg Esmolol 25 mg

5. Maintain Vital sign: Vital sign: BP: about 110/60 mmHg BP: about 110/60 mmHg HR: 90/min HR: 90/min SpO 2 : SpO 2 : 92% at the beginning 92% at the beginning 99% during operation 99% during operation Medication: Medication: Inhalation gas: Desflurane Inhalation gas: Desflurane Atropine: 0.5 mg Atropine: 0.5 mg Nitroderm Nitroderm

6. Emergence Medication Medication Atropine: 0.5 mg; Enlon:52 mg Atropine: 0.5 mg; Enlon:52 mg Vital sign Vital sign BP: 250/135mmHg BP: 250/135mmHg HR: 90/min HR: 90/min SpO 2 : SpO 2 : Rapid drop to 60% Rapid drop to 60% Respiration sound: Respiration sound: Bilateral rales Bilateral rales Heart sound: Heart sound: Severe systolic murmur (4/6) at left 5th intercostal space Severe systolic murmur (4/6) at left 5th intercostal space

7. Emergence Mask ventilation with pure O2 Mask ventilation with pure O2 Medication: Medication: Trandate, Millisrol (bolus and infusion), Lasix, Morphine, Solu-cortef Trandate, Millisrol (bolus and infusion), Lasix, Morphine, Solu-cortef Set A-line Set A-line Insertion of CVP (femoral vein) Insertion of CVP (femoral vein) Re-intubation Re-intubation ICU ICU

8. Induction Induction Emergence Emergence SpO2: 60% SpO2: 60%

9. Medication Medication BP BP Blood gas: Blood gas: PO2: 83.9mmHg PCO2: 58.6 mmHg pH: 7.22 SpO2: 93.6%

10. Chest X-ray Bilateral pulmonary edema; Bilateral rales Bilateral pulmonary edema; Bilateral rales Heart sound: Heart sound: Systolic murmur

11. 12 lead ECG At OR 16:20

12. Send to ICU Ventilator Ventilator SIMV SIMV PEEP PEEP Sedation Sedation

13. 12 lead ECG at ICU 17:38

14. Lab data at ICU CBC CBC WBC: 15340 WBC: 15340 Cardiac enzyme Cardiac enzyme CK, CK-MB, Troponin I: within normal range CK, CK-MB, Troponin I: within normal range Blood gas: Blood gas: (9/17) PO2: 192 mmHg (9/17) PO2: 192 mmHg (9/18) PO2: 177 mmHg (9/18) PO2: 177 mmHg Cardiac echo Cardiac echo LVEF: 70%, good LVEF: 70%, good

15. Discussion

16. Chest X-ray: before & after op

17. What happened? Pulmonary Edema

18. Etiology Types Types NEGATIVE-PRESSURE PULMONARY EDEMA (Permeability) NEGATIVE-PRESSURE PULMONARY EDEMA (Permeability) CARDIOGENIC PULMONARY EDEMA (Hemodynamic) CARDIOGENIC PULMONARY EDEMA (Hemodynamic) NEUROGENIC PULMONARY EDEMA NEUROGENIC PULMONARY EDEMA Which is most likely? Which is most likely?

19. NEGATIVE-PRESSURE PULMONARY EDEMA Also known as postobstructive pulmonary edema Also known as postobstructive pulmonary edema Characterized by its rapid onset and short-lived course Characterized by its rapid onset and short-lived course Large, negative intrapleural pressures are the pathophysiologic hallmark of negative-pressure pulmonary edema Large, negative intrapleural pressures are the pathophysiologic hallmark of negative-pressure pulmonary edema Various types of airway obstruction, including croup, epiglottitis, laryngospasm after tonsillectomy, hanging, and tumors have been reported Various types of airway obstruction, including croup, epiglottitis, laryngospasm after tonsillectomy, hanging, and tumors have been reported Symptoms commonly resolve within 12 to 24 hours Symptoms commonly resolve within 12 to 24 hours Suction mechanism Suction mechanism

20. NEUROGENIC PULMONARY EDEMA NEUROGENIC PULMONARY EDEMA The exact cause of neurogenic pulmonary edema is unknown The exact cause of neurogenic pulmonary edema is unknown Increased capillary hydrostatic pressure and increased capillary permeability Increased capillary hydrostatic pressure and increased capillary permeability With a history of head trauma or intracranial pathology With a history of head trauma or intracranial pathology CARDIOGENIC PULMONARY EDEMA CARDIOGENIC PULMONARY EDEMA Develops when Pcap is excessively high, overwhelming the ability of the lymphatic system to resorb fluid. Develops when Pcap is excessively high, overwhelming the ability of the lymphatic system to resorb fluid. Left-to-right shunting lesions, such as a patent ductus arteriosus or a ventricular septal defect Left-to-right shunting lesions, such as a patent ductus arteriosus or a ventricular septal defect Ventricular function Ventricular function

21. Negative-pressure Pulmonary Edema in a Child with Hiccups during Induction [CASE REPORTS] Anesthesiology, 93(1): 282-4 Negative-pressure pulmonary edema (NPPE) occurs soon after relief of acute or chronic obstruction of the upper airway. It is commonly reported after laryngospasm during induction or emergence from anesthesia. Negative-pressure pulmonary edema (NPPE) occurs soon after relief of acute or chronic obstruction of the upper airway. It is commonly reported after laryngospasm during induction or emergence from anesthesia. Markedly negative intrapleural pressures during airway occlusion cause increased venous return and increased left ventricular afterload. The increased hydrostatic pressure gradient in the pulmonary capillaries leads to transsudation of fluid into the alveoli. Hypoxemia and a hypoxia-induced hyperadrenergic state further promote edema formation. Markedly negative intrapleural pressures during airway occlusion cause increased venous return and increased left ventricular afterload. The increased hydrostatic pressure gradient in the pulmonary capillaries leads to transsudation of fluid into the alveoli. Hypoxemia and a hypoxia-induced hyperadrenergic state further promote edema formation. It is likely that more cases of unexplained perioperative hypoxemia are related to unrecognized NPPE. It is likely that more cases of unexplained perioperative hypoxemia are related to unrecognized NPPE.

22. Negative-pressure Pulmonary Edema in a Child with Hiccups during Induction [Correspondence] Anesthesiology, 94(2): 378-9 NPPE v.s. CPE: NPPE v.s. CPE: The most specific method for differentiating NCPE from CPE is the demonstration of increased alveolar – capillary permeability, which is characteristic of NCPE. Alternatively, pulmonary capillary wedge pressure measurement could be useful to differentiate CPE from NCPE. The most specific method for differentiating NCPE from CPE is the demonstration of increased alveolar – capillary permeability, which is characteristic of NCPE. Alternatively, pulmonary capillary wedge pressure measurement could be useful to differentiate CPE from NCPE. Echo: Echo: An echocardiogram shows normal left ventricular systolic and diastolic function in NCPE An echocardiogram shows normal left ventricular systolic and diastolic function in NCPE X-ray X-ray Centrally distributed pulmonary edema could be suggestive of cardiogenic origin Centrally distributed pulmonary edema could be suggestive of cardiogenic origin

23. Pulmonary oedema associated with airway obstruction Canadian Journal of Anaesthesia. 37(2):210-8, 1990 Mar Pathogenesis of pulmonary oedema associated with upper airway obstruction is multifactorial Pathogenesis of pulmonary oedema associated with upper airway obstruction is multifactorial negative intrapleural pressure is the dominant pathophysiological mechanism involved in the genesis of pulmonary oedema associated with upper airway obstruction negative intrapleural pressure is the dominant pathophysiological mechanism involved in the genesis of pulmonary oedema associated with upper airway obstruction The majority of cases present within minutes The majority of cases present within minutes Resolution is typically rapid, over a period of a few hours. Resolution is typically rapid, over a period of a few hours. Maintenance of a patent airway, supplemental oxygen, mechanical ventilation and positive end-expiratory pressure Maintenance of a patent airway, supplemental oxygen, mechanical ventilation and positive end-expiratory pressure

24. Thanks for your attention