Hypertensive disorder accounts for 10-15% of pregnancy.

Pregnancy indused hypertension[PIH]-

• Preeclampsia and Eclamsia syndrome
• Chronic hypertension without protinuria
• Chronic HTN with superimposed preeclampsia / eclamsia
• Gestational HTN or transient HTN of third trimester

Preeclampsia and Eclamsia syndrome:

Classical triad-

☛ Hypertension  ,protinuria    and    generalized edema after 20 wks of gestation
☛ If superimposed by convulsion called eclampsia.

Chronic  HTN :

☛ Present before 20 Wk and beyond 12 Wk
☛ When accomplished with preeclampsia called superimposed

Gestational HTN:

☛ Occur late in third trimester or post partum.
☛ Comes back to normal within 2 wks of delivery.
☛ Not associated with proteinuria or generalized edema.

 

Etiology

Exact etiology not known, It is a “disease of theories”.

☛ Abnormal placentation and failure of normal invasion of trophoblastic cells.
☛ Maladaptation of maternal spiral arteries.
☛ abnormal villous development and placental insufficiency.
☛ Imbalance of vasoconstrictor and vasodilatory substances.
☛ ↑ TxA2 and ↓PGE2, I2.
☛ The lowr resistance plasenta becomes high resistance due to inadequet trophoblastic invasion and maternal spiral artery remain tightly constricted.

Spiral artery of myometrium remain constricted
⟱
↓ 30% of uteroplacental flow
⟱
Placental trophoblastic relese mitogens and cause endothelial injury
⟱
Relese of “fibronectin”
⟱
Causes PG imbalance
⟱
↓PGE2 and ↑ Thromboxane

 

Fibronectin causes widespred endothelial damage and leads  to –

1. Placental insufficiency
2. Coagulation abnormality
3. Renal failure
4. Placental aggargation
5. loss of capillary integrity with leakage of fluids and proteins.

Pathophsiology-

Almost all system are affected due to widespred vasoconstriction and endothelial damage-

1) Cardiovascular system  [CVS]-

3 Sets of abnormalities can be presents

① High cardiac output, low to normal plasma volume, High SVR, low filling pressure
② Normal cardiac output,high SVR,loe filling pressure.
③ Highly elevated SVR , low blood volume, decresed left ventricular function.

Incresed blood pressure mainly because of ↑ CO rather than  ↓ SVR especially in early course.
↓ plasma volume  as much as 30%. Failure to increase plasma volume by 20-24 wks usually foretells Preeclampsia.

 

Red cell mass usually maintained.

☛ Hematocrit usually raised.
☛ ↓ in colloidal oncotic pressure due to ↓ plasma proteins.
☛ Salt and water retention.
☛ ↑ed circulating levels of Renin,Angiotensin, Catecholamine’s and ANF.

Pulmonary edema– vasoconstriction, endothelial damage, ↓ colloid oncotic pressure,↑ ed capillary leakage is responsible for leakage into extra vascular compartment and cause pulmonary edema.

Associated coagulation abnormalities:

☛ ↓ in platelet count- as much as ≤ 40,000
☛ Bleeding time is increased.
☛ Fibrin degradation product ↑ed.

 

HELLP Syndrome:

• Hemolysis: characterized by abnormal peripheral blood smear, increased bilirubin levels.
• Elevated liver enzymes- ↑ed  aspartate level ≥ 70IU/ L, LDH ≥600 U/L
• Low platelet count- ≤ 1LAC/MM³  CAN GO UPTO 25,000/MM³

Rate of fall of platelet count is more important, platelet generally return to normal after 72 hrs of delivery but can persist for longer period.

Patient c/o epigastric pain, nausea, vomiting, bleeding  episodes, hematuria.

Treatment; whole blood, FFP, platelets, plasmapharesis, supportive treatment of liver and kidney.

In fulminant cases, delivery of fetus irrespective of gestation.

2) Respirtory system-

• Airway edema due to retention of water into tissues, ↓ed plasma oncotic pressure,↑ capillary pressure
• Potential airway compromise
• Increased incidence of failed ventilation and intubation
• Reduced volumes and capacities
• depression Mgso4 therapy,sedatives and anti- convulsant t/t is on.
• Shift of O2 dissociation curve to left due to ↑ed levels of COHB, due to destruction of RBC’S.

Pul. Edema- ↓edoncotic pressure,↑ endothelial damage, ↑ capillary permeability.

     

3) Liver-

-Elevated liver enzymes

AST ≥ 70 U/L
LDH ≥ 600 U/L

– Generalised swelling and periportal haemorrhage causes epigastric pain, subcapsular haematoma.

4) kidney-  

☛ endothelial damage
☛ glomerular and tubular injury
☛ ↓RBF
☛ ↑ blood uric acid levels
☛ ↓ creatinine clearance,
☛ proteinuria
☛ oligourea →ARF
☛ permanent glomerular sclerosis may need permanent dialysis therapy.

 

5) Central nervous system-[CNS]

CEREBRAL EDEMA
⤋                                 ⤋
VASOGENIC           CYTOTOXIC

☛ Hyperreflexia, CNS irritability
☛ intacranial haemorrhage
☛ ↑ICT
☛ focal thrombosis and hemorrhage
☛ visual disturbances, retinal hemorrhage
☛ occipital blindness

 

6) UTERUS AND PLACENTA–

☛ uterus become hyeperactive and sensitive to oxytocin
☛ may cause uterine atony
☛ decresed uteroplacental blood flow.
☛ premature labour
☛ fibrin deposits and multiple infarcts
☛ abruption

 

7) FETAL MORBIDITY-

☛ Resp. distress,premature birth.
☛ IUGR
☛ Muconium aspiration

 

MANAGEMENT:

GOALS→

1. Minimise vasospasm by t/t of antihypertensive, Mgso4 and improvement in circulation
2. Improve intravascular volume
3. Reduce CNS hyperactivity
4. Correct acid base balance
5. Correct electrolytes imbalance
6. Early detection of coagulation,liver and kidney dysfunction.

Therapy→

1. Hospitalization,eclampsia room,
2. Bed restin left lateral position to improve uteroplacental circulation and avaoiding aortocaval compression
3. Adequate water and sodium intake to avoid Na depletion and thereby i↑ rennin-angiotensin production
4. Diuretics are routionly not recomonded unless there is pulmonary edema
5. Control of seizures amd management of airway in eclamptic patient
6. Mgso4 therapy and antihypertensives

Role of  Anaesthetist→

1. Intensive care management
2. Control of airway
3. Cardiac monitoring
4. Support of ventilation
5. Labour analgesia
6. Elective/ emergency caesarian section
7. Neonatal resuscitation

Mgso4 Therapy:

Uses- prophylactic therapy to prevent eclampsia and for treatment of eclampsia.

Mechanisum of action→

1. Vasodilation- Non- sedative vadilatory action,improves cerebral,renal and utoro-placental circulation, mild anti- hypertensive action, reduces rennin and angiotensin activity. Attenuates vascular responses to  presser substances.
2. Tocolysis- ↓ uterine activity and improvesuterine blood flow
3. Potent cerebral vasodilator- works better than other anticonvalsant.
4. ↑ prostacycline relese by endotheline cells and by ↓ platelet aggregation.

Dose→

1. 4 gm i.v 20% solution bolous over 10 min followed by 10 gm 50% i.m, 5 gm in each buttock and 5gm  every 4 hrly alternatively in each buttoks.
2. 4gm iv over 10 min followed by iv infusion 1gm iv.

Monitoring→

☛ Urine output ≥ 25 ml/hr
☛ Knee jerk +
☛ RR ≥ 12/MIN

 

Mg levels→

☛ THERAPEUTIC LEVEL- 4-8 MEQ/L
☛ ECG changes- 5-10 ( wide qrs,prolonged PR )
☛ Loss of deep tendon reflex- 10 meq/l
☛ SA nodal and AV nodal block- 15 meq/l
☛ RESP. paralysis- ≥ 15
☛ Cardiac arrest – 25

 

Side effects→

1. Muscle weekness – Due to decrese relese of Ach at motor nerve ending, ↑ed sensitivity to non- depolarizing muscle relaxant and there potentiation.
2. Respiratory insufficiency-
3. Neonatal effects- mg readialy crosses placenta,low apgar score, decresed muscle tone,resp depression/Apnea.

Anti- hypertensive agent:

☛ Hydralazine: 5-10mg i.v,slow onset 20-30 min. Duration- 2-3 hrs, causes fetal distress.
☛ Alpha- methyl dopa: 250 mg qid/tds

Beta- blockers:

LABETOLOL  → Start 20 mg i.v upto 1-3 mg/kg, onset 1-2 min,duration- 2-3 hr. increases uterine and placental blood flow.

NIFEDIPINE → 5-10 MG SUBLINGUAL/ORAL

Maternal sequalae of HTN:

CVA,HELLP, Convulsion, Occipital blindness, pul. Edema,  Renal failure.

Check list before instituting epidural block/spinal anesthesia :

1. Working large bore i.v line
2. NBM status
3. Coagulation profile should be normal.
4. Control of hypertension
5. Hydration status
6. Urine output in 24 hrs
7. Last dose of Mgso4/ antihypertensive
8. Airway examination.
9. Aspiration prophylaxis
10. Probe oximeter and o2 supplimentaion
11. Left lateral tilt

Recommended techniques of general anaesthesia for caeserian section:

1. Aspiration prophylaxsis– H2 blocker,Non- particulate antacids,Metoclopramide
2. Routine monitoring – ECG,SpO2,EtCO2,nibp,SUCTION EQUIPMENT,Aids for difficult intubation should be kept ready, NM Monitoring, Antihypertensive and inotrops should be available.
3. Left lateral displacement of uterus.
4. Preoxygenation with 100% O2 for 3-5 min
5. Cricoids pressure after induction
6. Give drug to blunt pressure response
7. Facilitation of intubation with succhynylcholine and maintain cricoids pressure till ET T ube cuff is inflated.
8. Ventilate with 50% o2 + 50% N2O and volatile anesthetic as necessary
9. Maintain normocarbia and use of muscle relaxation as necessary vec/atracurium.
10. Neuromuscular monitoring if patient of Mgso4
11. After delivery,↑ N2o to 70% discontinue or reduce volatile anesthetic.
12. Administer BZP and opioids ,oxytocin to drip
13. Insert nasogastric tube before sx.
14. Reverse neuromuscular blockeds after reflexes +.
15. Extubate the patient awake,obeying commands with after adequate reversal of NM blocking agents.                                                                                                                                                                                                              Dr.Nagesh