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ARTICLES
It was the year of 1999, when , for the first time I got an honour of presenting two articles for my clinical group. Co-inceidently both assignments (presentations), namely PIH (Pregnancy Indcuced Hypertension) and Complications of Cesarian section , were related to Gynaecology and Obstetrics. Here I am pasting the first artcile which I created for the very first occaasion . I'll be glad if it could be helpful to any of the Gynae students .
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ECLAMPSIA
Introduction It is a serious complication and late menifestation of acute toxemia of pregnancy .It is a Disease of theories as despite of extensive theories , exact cause is still unknown .For example the synonym "Toxemia Of Pregancy", shows its possible relation with toxin of infectious agent.
Definition Addition of grandmal seizures to mild / severe pre-eclampsia
Pre-eclampsia ( Pregnancy induced Hypertension) Specific disease of pregnancy charecterized by any 2 of the following clinical features. Edema, Hypertension and Proteinuria, after 28 weeks of gestation.
BIOSTATISTICAL DATA
Incidence is inversely proportional to standard of ante-natal care.
Prognosis 100 % preventable disease by good ante-natal care .Under good treatment and appropriate nursing care prognosis is very good.
Maternal mortality = 3 - 4 %
Perinatal mortality = 30 - 40 %
25 % Antepartum
50 % Intrapartum
25 % Post partum
AETIOLOGY
Still Unknown but there are some theories like.....
1- Immunological Mechanisms Role of HLA , ABO and tissue specific antigens.
2- Altered Vascular Reactivity Role of renin which is produced by JG apparatus of kidney, placenta and fetal kidney .Helps in production of angiotensin 2 .In Eclampsia as there is dec. conc. of production of local vasodilatory prostacyclin so effect of angiotensin 2 is increased.
3- Theory Of Coagulation Disturbance There is a decrease in number of circulating platelets , increase in fibrinogen products and decrease in fibrinolytic activity .These all things how occurance of DIC.
Beside these theories there is some evidence of relation with inadequate intake of protein and calcium .
RISK FACTORS
Nulliparity Occurs usually in 1st pregnancy
Age extremes ( less than 20 yrs, more than 34 yrs )
Multiple Gestation (pregnancies)
Hydatidiform Mole
Diabetes Mellitus
Non Immune Fetal Hydrops
Ch.Hypertension
Ch.Renal Disease
CHARECTERISTIC PATHOLOGY
Cerebral Lesions Due to inc. intra cranial pr., brain becomes edematous.
Hepatic Lesions are diagnostic .Necrosis in periphery of lobules gives yellow coloured areas.Hemorrhages around portal canals give red coloured areas.
Renal Lesions there is renal glomerular endotheliosis, there is a swelling of endothilial cells of capillaries.
PATHOGENESIS
a- DIFFUSE VASOSPASM Produces :-
1- loss of normal state of pregnancy against effects of renin, angiotensin 2 and aldosterone ===> Systolic and diastolic Hypertension.
2- Inc. Capillary Permeability === > Hemoconcentration === > Inc. BUN, Creatinine , Uric Acid, Hb .
3- Inc.Cap. Permeability === > Edema , Obesity
b- CAPILLARY WALL ENDOTHELIAL INJURY
Produces Microangiopathic hemolytic anemia , Platelet destruction, DIC,
CLINICAL MENIFESTATIONS
Weight gain gain of more than 0.75 k.g / week
Edema initially at ankles then fingers and eyes.
Hypertension
Proteinuria
Oliguria
Convulsions
These are grandmal epileptiform fits having following stages:-
a-Aura visual phenomenon in which light flashes appear before eyes.
b- Cry due to laryngo-spasm
c-Tonic Phase Unconsciousness, cyanosis, gen.muscle spasm.
d- Clonic Phase Violent motility e.g.Tongue is bitten, inhalation of vomiting, cerebral hemerrhage, hypoxia
Other menifestations of Eclampsia include :- Occipital or frontal Headache, Flashes Of Light Before Eyes, Epigastric Pain , Vomiting, Muscle Twitching
COMPLICATIONS
Asphyxia, Vomit Inhalation, Acute left Vent. Failure, Pulmo-edema, Sepsis, Br.Pneumonia, Cerebral Hemorrhage, Renal Failure, Liver Failure,
Causes Of Maternal Death
Immediate Death Is Due To Anoxia, Apoplexy , Acute left Vent. Failure, Lung collapse,
DeathWithin 3 Weeks Is Due To Infection, Uremia, Pneumonia
Death Within 3-4 Weeks Is Due To Hepatic Coma
Death Within 1-2 years Is Due To Ch.Renal Failure
HELLP Syndrome
Uncommon but fatal variant of pre-eclampsia associated with Hemolsysis, Elevated Liver enzymes, Low Platelet count. Unlike pre-eclampsia it is found in multiparaand in greater than 25 yrs. of age.
DIAGNOSIS
Presence of pathologic edema (hands , face) proteinuria. Hypertension is essential.
Differential Diagnosis Epilepsy , Tetanus , Strychnine Poisoning, All causes and types of Coma, Hysteria
TREATMENT
PROPHYLAXIS Minidose of Aspirin (less than 60 mg / day) as it inhibits prostaglandin synthetase -------Inhibition of Thromboxane .It should be started b/w 10-12 weeks of gestation.But It can inc. possibility of Abrup.Placenta .
CLINICAL APPROACH
A- Immediate Treatment Aim is to prevent further fits.So heavy sedation immediately like Magnesium sulphate ( I.V ). Initially 4-5 g for 20 mins , then, 1-3 g / hr.
- keep the patient in silent, dark room .
-a mouth gag should be put b/w teeth to prevent tongue from bitten and air-way inserted.
- Oxygen administration and suction of naso-pharaynx.
B- Medical Treatment
-Good Nursing Care To prevent CNS stimulation, ext . stimuli of sound, light and tactile, should be reduced as much as possible. To Prevent Pneumonia , turn the patient from side to side / 2 hrs after sedation.Catheter sould be passed after sedation , as full bladder can act as stimulus for further fits.
-Sedation By ......Valium 10 mg (I.V) stat, Morphine (I.V), Chloral Hydrate per rectum, Na-Thiopentone , Haloperidol 5 mg (I.V)
-Hypotensive Drugs When B.P is 120 mmHg, drugs like Veratone (0.6 ml) I.M / 15 mins are given to prevent brain hemorrhage.
C- Obstetrical Treatment
-If patient is unconscious , note onset of labour by :-Restlessness of patient, contraction of uterus.
- Rupture the membranes artificially after sedation .
- Apply forceps in 2nd stage of labour to avoid fits.
-Caesarean Section , tough contraindicated , but rarely used when medical treatment becomes unable to stop fits.
An Article By Syed Ikram Hussain Abidi
Presented by Dr.Ikram, Dr.Mehwish and Dr.Kashif
to Prof.Dr.Meher (MBBS,FRCOG)
Gynae Unit 1 , Civil Hospital Karachi