Mendelson syndrome,Amniotic fluid embolism,HELLP syndrome

LikhithaNalluru 1,049 views 48 slides May 20, 2024
Slide 1
Slide 1 of 48
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40
Slide 41
41
Slide 42
42
Slide 43
43
Slide 44
44
Slide 45
45
Slide 46
46
Slide 47
47
Slide 48
48

About This Presentation

mendelson syndrome,hellp syndrome,amniotic fluid embolsim


Slide Content

1

Mendelson syndrome hellp syndrome amniotic fluid embolism By : Dr Nalluru Likhitha (MD Anaesthesia) Moderator: Dr Sudha Madhuri , Asst Professor MD Anaesthesia NRIIMS, Sanghivalasa 2

Mendelson syndrome 3

introduction It is called as Aspiration pneumonitis . It is a chemical injury caused by inhalation of sterile gastric contents. It occurs around 10% of patients who are hospitalised after a drug overdose. Occurs in approximately 1 of 3000 operated patients in which general anaesthesia is administered and accounting for 10-20% deaths assosciated with anesthesia . In 1956 , Mendelson first showed that acidic gastric contents introduced into the lungs of rabbits caused severe pneumonitis and reported in patients who aspirated while receiving general anesthesia during obstetrical procedures. 4

Feature Aspiration pneumonitis Aspiration pneumonia Mechanism Aspiration of sterile gastric contents Aspiration of colonised oropharyngeal material Pathophysiological process Acute lung injury from acidic and particulate gastric material Acute pulmonary inflammatory response to bacteria and bacterial products Bacteriological findings Initially sterile with subsequent bacterial infection possible Gram positive cocci,gram negative rods and rarely anerobic bacteria. Chief predisposing factors Markedly depressed level of consciousness Dysphagia and gastric dysmotility. Presentation Patient with a history of depressed level of consciousness in whom a pulmonary infiltrate and respiratory symptoms develop. Institutionalised patient with dysphagia in whom clinical features of pneumonia and an infiltrate in a dependent bronchopulmonary segment. Clinical features No symptoms or symptoms ranging from a non productive cough to tachypnea , bronchospasm ,bloody or frothy sputum and respiratory distress 2 -5 hrs after aspiration. Tachypnea , cough and signs of pneumonia. 5

Predisposing factors 1. Physiological changes during pregnancy : Slowed GIT transit due to: Increased progesterone and gastrin Reduced motilin Mechanical displacement by pylorus by gravid uterus Increased gastric volume Increased gastric acidity due to gastrin Decreased gastroesopheal sphincter tone Gastroesophageal reflux: Twin pregnancy Hydraminos Gross obesity that increase gastric pressure to 40cmH2O 6

PREDISPOSING FACTORS 2. Risk of volume and pH Severity of lung injury increased significantly as the volume of the aspirate increased (20 to 25ml in adults) and its pH decreased (<2.5). Aspirate of particulate food matter may cause severe pulmonary damage even if the pH of aspirate is >2.5. Aspiration of gastric contents results in a chemical burn of the tracheobronchial tree and pulmonary parenchyma ,causing intense parenchymal inflammatory reaction. 7

Predisposing factors 3. Loss of airway reflxes : increased aspiration during failed intubation. More common during emergency induction of general anesthesia . 4. Choice of Anesthesia technique: Deep sedation > GA > RA RA may cause aspiration due to LA toxicity that causes convulsions and CNS depression , supine hypotension induced nausea and vomiting. 8

Predisposing factors 5.Other factors: Labor related nausea Pain , fear. Obesity Polyhdraminos Twin pregnancy Recurrent food ingestion Drugs as opiods , benzodiazepines,sedatives ,magnesium sulphate etc. 9

Pattern of lung injury Biphasic pattern : The first phase peaks at one to two hours after aspiration and results from the direct caustic effect of aspirate on the cells lining the alveolar capillary interface. The second phase which peaks at 4-6hrs is assosciated with infiltration of neutrophils into alveoli and lung interstitium . 10

Signs and symptoms Wheezing Coughing Shortness of breath Cyanosis Pulmonary edema Hypotension Hypoxia Severe ARDS and death Silent aspiration manifests only as arterial desaturation with radiological evidence of aspiration. 11

Clinical staging Stage 1 Profound dyspnea Tachycardia Bronchospasm with normal xray Stage 2 Increasing cyanosis and hypoxemia Minor xray findings Stage 3 Profound hypoxemia Reduced compliance Diffuse bilateral infiltrates on xray Stage 4 ARDS 12

Investigations: Gastric aspirate analysis. ABG for PaO2 , hypercarbia. CXR : soft mottled densities in peripheral dependent areas of lungs. occurs 10-12hrs after aspiration. Snow Storm Appearence 13

treatment Airway : Turn patient to side and head down position. Suction mouth and posterior pharynx. Intubate with cuffed ETT. Suction ETT several times after intubation. Ventilate Ventilate with 100% o2 between suctioning. Use minimum required FiO2 as it increases lung injury. PPV 14

TREATMENT Fibreoptic bronchoscopy: Through ETT to remove smaller particulate matter. Bronchoscopy to remove solid material and rexpand atelectotic segments. Send gastric aspirate for culture , pH. Others : Antibiotic therapy according to culture and sensitivity reports. 15

Complications Lung abscess Necrotising pneumonia Empyema 16

Prevention of aspiration Antiaspiration prophylaxis: NPO for 6-8 hrs. Oral antacid therapy : 0.3 M sodium citrate (nonparticulate) Sodium bicarbonate H2 Antagonists : 150 mg Ranitidine or 300mg Cimetedine PO night before surgery. Dose repeated 1-2 hrs before induction. 50mg Ranitidine IV 30mins before emergency caesarean section. 17

Prevention of aspiration Proton pump inhibitors : Omeprazole 20-40mg PO Lanzoprazole 15-30mg PO Prokinetics : Metaclopromide 10mg PO/IM/IV 1hr before surgery for oral and IM , 1-3mins before induction for IV. Anticholinergic therapy : Glyco /Atropine/Scopolamine. Nasogastric tube , decompress stomach is distended before extubation . 18

Prevention of aspiration Avoid loss of consciousness: Avoid GA when alternatives present. Avoid oversedation Avoid hypotension of regional anesthesia and aortocaval compression Avoid LA toxicity. 19

Prevention of aspiration Appropriate GA techniques: Assume all second trimester patients are at increased risk of aspiration. Trained assistant for induction mandatory. Cricoid pressure from before loss of consciousness to cuff inflation. Use of cuffed ETT. Extubate only when fully awake. 20

Prevention of aspiration Appropriate position : Headup position causes increased chances of aspiration if vomiting occurs. Supine with right hip elevation by 10-15 degree is ideal. Support head on small pillow in sniffing position. During extubation : lateral head down position. 21

HELLP Syndrome 22

introduction The acronym HELLP syndrome was coined by Weinstein in 1982 to describe a syndrome consisting of Hemolysis,Elevated liver enzymes and low platelet count. It is life threatning obstetric complication usually considered to be a variant of pre eclampsia. Both conditions usually occur during the later stages of pregnancy or sometimes after childbirth. 23

causes 24

25

Clinical features Right upper quadrant pain and epigastric pain Nausea Vomiting Headache Hypertension Proteinuria 26

Diagnostic criteria Hemolysis : abnormal peripheral blood smear. Elevated liver enzymes: Increased LDH>600IU/L Increased AST >70IU/L Thrombocytopenia : PC<1,00,000/mm3 27

complications Maternal Fetal DIC Placenta abruptio Acute renal failure Pulmonary edema Pleural effusion Cerebral edema Severe ascites Retinal detachment Laryngeal edema ARDS Maternal death Cerebral hemorrhage Perinatal death Preterm delivery Neonatal thrombocytopenia Respiratory distress Intrauterine growth restriction 28

management 29

Anaesthetic management Preoperative : ECG CBC LFT RFT PT and APTT Blood components including cross matched red cells , platelet concentrates and plasma should be available. Urinary cathetrisation . 30

Choice of anesthesia Clinical situation : raised ICP clinical evidence of bleeding coagulopathy PC<80,000 hemodynamic instability maternal or fetal compramise yes no General anesthesia Regional anesthesia 31

Neuraxial analgesia for labour It is recommended for several reasons: Avoid GA and the possibility of airway castotrophe and marked hypertension with laryngoscopy in the event of emergency caesarean delivery. Optimise the timing of epidural catheter placement in the setting of a declining platelet count. 32

Lumbar epidural analgesia Advantages include: High quality of analgesia which attenuates the hypertensive response to pain. Reduction in levels of circulating catecholamines and stress related hormones. Possible improvement in intervillous blood flow. If there is no signs of intraspinal bleeding , catheter should be removed as soon as possible. 33

General anesthesia Involves high materno fetal anesthetic risk. Indications : Severe ongoing maternal hemorrhage Sustained fetal bradycardia Severe thrombocytopenia and coagulopathy Pulmonary edema Altered level of consciousness 34

General anesthesia Considerations : IBP should be initiated before induction of GA. Difficult airway equipment should be made readily available. Supine position with left uterine displacement. Rapid sequence intubation. Avoid repeated attempts , proceed with SGA before airway is irretrievably lost. 35

Amniotic Fluid Embolism 36

introduction Amniotic fluid embolism is a life threatening obstetric emergency. It happens due to sudden gush of amniotic fluid , fetal cells , hair and amniotic debris entering the maternal circulation. Also called as Obstetric shock or Anaphylactic syndrome of pregnancy. 37

Risk factors: Older age Abruptio placenta Eclampsia Multiple gestation Induction of labour Artifical or spontaneous rupture of membranes Operative delivery 38

39

40

41

System Signs and symptoms Neurological Restlessness Confusion Seizure Respiratory Cough Dyspnea Hypoxia Respiratory arrest Pulmonary edema ARDS Cardiac Hypotension Tachycardia Cardiac arrythmias Cardiac arrest Hematological Hemorrahage DIC Obstetric Fetal distress Uterine atony 42

diagnosis Clinical tests: Decreased O2 saturation in pulse oximetry. Decreased Etco2. ECG : Arrythmias , MI , asystole CXR: normal / effusion / cardiomegaly /pulmonary edema . ABG: reduced p02 and sO2 . TEE 43

DIFFERENTIAL DIAGNOSIS Anesthetic related Pregnancy related Other causes High /total spinal anesthesia Local anesthetic toxicity Pulmonary aspiration of gastric contents Uterine rupture Uterine atony Placental abruption Peripartum cardiomyopathy Eclampsia Air embolism Pulmonary embolism Sepsis Anaphylaxis Arrythmia Myocardial infacrtion Transfusion reaction CVA 44

Management : Airway Administer 100% oxygen. Intubate and support ventilation as needed. Cardiovascular support Start chest compressions if needed. Ensure left uterine displacement to relieve aortocaval compression. Administer fluids and vasopressors. Establish large bore intravenous access. Consider invasive blood pressure monitoring. 45

Management Fetus : Monitor fetal well being. Perimortem caesarean delivery. Hemostatic support : Activate the obstetric hemorre protocol and massive transfusion protocol. Send blood for serial lab assessment to monitor for coagulopathy and electrolyte disturbances. Provide blood component therapy as indicated. Ensure normothermia Postresuscitation care : Notity ICU. Consider mild therapeutic hypothermia after cardiac arrest. 46

references Miller’s 9 edition Chestnut obstetrics anaesthesia – 6 th edition Barasch clinical anesthesia – 8 edition Morgan and Mikhail’s 6 edition D. B. Scott, MENDELSON'S SYNDROME, BJA: British Journal of Anaesthesia , Volume 50, Issue 10, October 1978, Pages 977–978, https://doi.org/10.1093/bja/50.10.977 D Leslie, RE Collis, Hypertension in pregnancy, BJA Education, Volume 16, Issue 1, January 2016, Pages 33–37, https://doi.org/10.1093/bjaceaccp/mkv020 Jatin D. Dedhia , Mary C. Mushambi , Amniotic fluid embolism, Continuing Education in Anaesthesia Critical Care & Pain, Volume 7, Issue 5, October 2007, Pages 152–156, https://doi.org/10.1093/bjaceaccp/mkm031 47

48