Postpartum Collapse

Postpartum Collapse

          Postpartum maternal collapse is a frightening obstetric complication. Majority of these cases occur as a result of haemorrhage which is revealed. However, if the patient has lost no more than 0.5 – 0.75 L of blood and yet is collapsed, either she is losing blood internally or other shock- producing factors are operative. In the first instance, the most likely sites of bleeding are within the body of the uterus it self, the peritoneal cavity and the retroperitoneal spaces.

          A uterus which is slowly filling with blood may often be fairly hard and the impression of sixe on palpation is more important than the actual height of fundus. Quite large quantities of blood can lie in the peritoneal cavity without producing significant physical signs locally, although general signs of shock are obvious. Pain is often much less than would be expected, and abdominal rigidity is usually absent in a postpartum case. Tenderness may be very indefinite, and the most noticeable features may be indefinite, and the most noticeable features may be bulging of the flanks, dullness to percussion and the patient's clear dislike of lying down flat and thereby allowing the blood to run up under the diaphragm. Many haemorrhages into layers of the broad ligament are overlooked if not large, but they add to the patient's shock.

          Only a small minority of cases of collapse after delivery occur without obvious vaginal bleeding, but these are the ones which pose a greater challenge for diagnosis and management. The management of postpartum haemorrhage has already been discussed in detail in Chapter 32 the pathopshysiology and aetiology of non haemorrhagic shock will be addressed here.

1)       Obstetric Haemorrhages :

1)       Obstetric Emergencies :

A)      Haemorrhagic Shock               Atonic PPH 

                                                           Traumatic PPH

B)      Non Haemorrhagic shock

          1)       Acute Inversion of the uterus

          2)       Amniotic fluid embolism

          3)       Pulmonary Thromboembolism

          4)       Air embolism

          5)       Rupture uterus

          6)       Mendel sons  syndrome (Inhaled vomit syndrome)

          7)       Cardiac Arrest

          8)       Acute Pulmonary edema

          9)       ARDS

          10)     Sepsis syndrome

Pathophysiology of Haemorrhagic shock:   

2)       Ion-donated

Pathophysiology of Non- Haemorrhagic shock     :

          Blood flow greatly reduced in a shock patient

          Cause – Vasoconstriction

                     diversion of blood from nonvital to vital              

          Brain  spared , skin – blood flow

Muscle blood flow. Leads to pallor & coldness       

Effect an Kidney :

          - Renal filtration ceases when systolic  Bp 80

            resulting  to anuria

           The duration of uncorrected shock will largely determine  the recovery

           of renal function

Effect on Heart:

          The heart is operating  under grave handicap

1)       The venaus return is reduced.

              Therefore and  atrial filling is poor so that cardiac  output falls, a              even  acceleration of the heart cannot compensate because of the  

             poor stroke volume.

2)       Sympathetic activated.

                   Result in to the

          Vasoconstriction & Tachycardia  in case of  Haemorrhage   by preventing further blood loss  so that the Blood supply maintain the too the vital centers;  but  where  shock    without  blood loss occurs, this  mechanism may be harmful by embarrassing the Heart action through  poor  veneus return  & thus precipating cardiac failure.

          Initially, there is a fall in pulse pressure.

          Because Diastolic Pressure is increased due to vasoconstriction & the systemic pressure to maintained for sometime.

          As the condition worsens

 

Vasoconstriction begins to fail                    At the sometime meanwhile

                                                                   Heart becoming  more inefficient .

          and both systolic & diagnostic pressure falls together. The awareness of pain is for same unknown reason dulled.

Other Autonomic effects:

1) Dilatation of stomach, ascending colon & the proximal half of the Transverse colon. comerpading to the predominant sympathetic nerve supply to the intestinal tract.       

Effect on Pitilury:

Anterior lobe of the pituitary is very susceptible to damage during pregnancy.

Necrosis occurs after P.P.H. or stocle

 

Hypothyroidism             Adrenal failure                Hypogonadism

 

                                                                             Prolaction & G.H.

                                                                             deficiency

All these is called a Sheehan's syndrome.

                                

Effects:

          The Immediate effects are less noticeable & serious than the remote failure to lactate & resume menses after the delivery.

8% Hypopititurism:

* Acute

Gential atrophy & Infertility

mild cases of Hypopititurism may occur in few cases.

Treatment includes hormone replacement with physiologic doses of Glucocorticoids, levothyroine, & sex steroids doses during periods of stress.

Acute Inversion of the uterus:

* Defn

* Causes:

          - Improper conduct of third stage by pulling on the card before                    placental separation.

          - 15% of cases of acute inversion occurs spontaneously & for no                  apparent reason.

Complete Inversion or the IIIrd degree is the ravest variety and it is with the lesser degrees of inversion that such causes of collapse may be overlooked.

* Abdominal Palpation is must to know the height and shape of the fundus & in cases of obesity a vaginal examination is must to diagnose the condition detail is discussed in the chapter of ____________________

Amniotic Fluid Embolism (AFE):

          - AFE is a life threatening complication of pregnancy with high mortality rate. It is first described in 1926 (*3), but its'real significance as a killer disease was probably recognized in 1941 when Steiner & Lushbaught *4 published an autopsy series of eight pregnant women who died of sudden shock during labour.

          - The mortality rates have fortunately decreased from 80 – 90% in the 1970 *5 to less than 30% in the more recently reported population based studies, *5 but besides mortality, there is a high incidence of neurological impairment in those who survive.

Pathogenesis:

          The Pathogenesis of the condition is not clear, Amniotic fluid probably enters the maternal venous circulation through breach in the barrier between the maternal vasculature & the amniotic fluid, most likely from the placental site or at the site of uterine trauma after the membranes have ruptured.

          Amniotic fluid embolic containg of liquer amni such as epithelial squonous, fat, meconium Lanugo hairs & meconium

Provokes

                                                                  

Immunological                         Humoral regn. in mother

Inflammatory Cascade

Multiorgan failure & DIC

The maternal response to amniotic fluid in many ways resembles an anaphylactic reaction and it has been suggested that the condition should be renamed as the “Anaphylactoid disease of pregnancy”.

Clinical Presentation:

·         Sudden onset of maternal collapse associated with tachypnoea, cyanosis, hypotension, altered Mental Status and disseminated Intravascular Coagulation (DIC).

·         However there may be prodormal phase in which the patient may be restless & exhibit altered mental state.

·         Atypical presentations include features of acute fetal distress or DIC without the symptoms of hypoxia and shock.

·         A possibility of AFE must be considered whenever a woman becomes unwell around the time of delivery or a baby shows sudden unexplained deterioration or born poor in condition. It is worthwhile observing such a patient for the next 24 hours and checking here coagulation profile.

Rapid deterioration and death occurs in most patients in the first one hour of the onset of symptoms 8.   Those who surview tend to manifest constitutional symptoms like fever with chills, nausea, vomiting.

Encephalopathy occurs commonly due to cerebral hypoxia causing confusion, agitation, seizures.

Diagnosis:

The diagnosis of AFE is essentially clinical and one of exclusion. It should be suspected in any Patient with sudden collapse during labour or Immediately after.

In a study by clark & associates (1995) fetal elements were detected in 75 percent autopsies and in 50 percent of specimens prepared from concentrated buffy coat aspirates taken antemortum from a pulmonary artery catheter, further, several studies have demonstrated that squamous cells, trophoblasts and other debris of fetal origin may commonly be found in the central circulation of Women with conditions other than amniotic fluid embolism. Thus, this findings is neither sensitive nor specific and the diagnosis is generally made by identifying clinically charaterth  sign and symptoms.

There is no specific labarotary test to diagnose AFE but post-mortem findings of amniotic fluid contents in the pulmonary vessels is perhaps the best proof so far of diagnosis of AFE (fig. 32.1 & 32.2)

Immunostaining techniques using Monoclonal TKH – 2 antibodies to demonstrate Mechanism and mucin (found in amniotic fluid) in maternal blood and lung tissue may increase the sensitivity of the diagnosis over the conventional stains (8).

Increased blood levels of zinc, coproporphyrin 10 a component of amniotic fluid and tryptase which is released due to degranulation of mast cells thereby suggesting on anaphylactic kind of reaction to fetal antigens”.

Management:

Obstetric Care

 

Pulmonary Thromboembolism:

Pulmonary embolism is one of the leading causes of direct maternal deaths in the western world 13.

          Pregnancy is a known hypercoagulable state. So women are at a higher risk of venous thromboembolic disease in pregnancy and puerperium compared to their non-pregnant counterparts the risk increase during the postpartum period due to endothelial injury that occurs during delivery.

          Pulmonary embolism should be therefore a major consideration in a patient who collapses suddenly in the postpartum period.

Etiology:

Pulmonary embolism occurs due to a thrombus blocking a pulmonary artery. The symptoms depend on the size of thrombus blocking a pulmonary artery & thereby the area of the lung which is not perfused.

Clinical presentation:

Symptoms:

Sudden onset dyspnoea, chest pain and features of collapse like tachycardia, cold clammy skin and syncope chest pain may occure any where in the chest and may radiate to the shoulder, arm or jaw. It is often associated with cough & Haemoptysis.

Diagnosis:

Diagnosis is easier in a woman with clinical suspicion of Deep Vein Thrombosis (DVT). There may be redness, swelling and tenderness over a vein in one of the legs suggesting DVT. However, pulmonary embolism may occur with an asymptomatic DVT. Screeing for Thrombophilia is must in high risk cases, Good Institute treatment reduces the fatality rate.

Low molecular weight heparin is safe during pregnancy and is not secreted in breast milk. Anticoagulation must be continued for three to six months with either LMWH 16.

Air Embolism:

An air embolus may be introduced in the course of intrauterine manipulation that has been preceded by some placental separation a lethal embolism may follow a bolus of 3 to 5 ml /kg of air 17.

Symptoms:

The typical symptoms are tachypnoea, chest pain and gasping. The diagnosis may be facilitated by precordial Doppler monitoring, transoesaphageal echocardiography, or if air is aspirating from a right heart catheter.

Management:

Immediate first-aid procedure is to place the patient in the head-down, lateral position in the hope of displacing the bolus of air towards apex of the right ventricle.

In case of smaller volumes of air now in the right side of the heart it may be possible for pulmonary circulation to continue until the air bubble is gradually passed piecemeal and less dramatically into the pulmonary system.

Management includes aspiration of air, discontinuation of nitrous oxide, administration of 100% oxygen and flooding the surgical site with saline to avoid further air entry.

Rupture Uterus:

When the delivery has followed operative Intervention, such a possibility is even more probable. It is a condition that carry’s high mortality if neglected through faitiure to diagnose it, and even when treated still remains one of the worst hazards of child bearing.

A previous caesarean section scar particularly of the classical variety should arouse one’s suspicions of uterine rupture in a case of collapse

Difficult forcep applications, those involving rotating of head Instrumental deliveries, any major manipulative procedure carry obvious risk of Inflicting rupture. The diagnosis is by no means easy, particularly in incomplete rupture, but if the shock persists inspite of adequate blood transfusion laparotany should be performed.

Mendleson’s Syndrome:

·         Gastric contents which are highly irritant may be inhaled during induction of anaesthesia.

·         In late pregnancy there is high chance of mendleson’s syndrome because of regurgitation of gastric contents and in obese patients where there is difficult intubation.

Clinical Features:

May appear in between 2 – 5 hours after anesthesia and include cyanosis, tachycardia, dyspnoea, wheeze, crepitant rales and decreased arterial oxygen tension.

Differential Diagnosis:

Amniotic fluid embolism, Acute pulmonary edema due to mitral stenosis and cardiac failure.

Cardiac Arrest:

·         Table 32.1

·         Pangraph

Acute Pulmonary Edema:

The incidence of pulmonary edema complicating pregnancy averages about 1 in 500 to 1000 deliveries at tertiary referral centers.

Causes:

·         Table 42.5 (pg. 929)

Cardiogenic Hydrostatic Edema: pg. 929

Acute Respiratory Distress Syndrome:

Defn: Pg. 930

Pathophysiology:

Acute Lung injury

Recruitement of Neutrophils to the site by chemokines

As Neutrophils accumulate               release cytokines.

                                                Further Injury to Endothelia Microvascular

Injury to Alveolar epithelium & Pulmonary Vascullalne

 

  Pulmonary Capillary Permeability   Surfactant      Lung        Areterial

                                                          inactivation   volume      Hypoxemic

2^nd phase of Syndrome Starts 3 – 4 days later:

1)   It involves development of fibrosing alveolitis & Subsequent repair.

Despite of all these, the long – term prognosis for pulmonary function is surprisingly good. (Herridge & Collagues, 2003) the subject has been reviewed by Wheeler and Bernanard (2007).

Causes:

·         Table 42.6