Zawadi Saidi, aged 22 years was a housewife, husband was unemployed. She lived in Utange area near Shanzu in Kilifi district. She was admitted in the labour ward at the Coast Provincial General Hospital on 6/4/2011 at 10.34PM as a referral from a private clinic. On admission, she was in poor general condition. She had laboured breathing and complained of headache, dizziness and palpitations, which had lasted about one week. Her parity was 3+0 gravida 4. Her last menstrual period was on 20/7/2010 and expected date of delivery 27/4/2011, hence gestation was 37 weeks on admission.
She had attended her first antenatal clinic visit at a gestation period of 30 weeks. During the visit, antenatal profile revealed haemoglobin level of 7g/dl, urine and stool analysis was normal. HIV test and Khan Test were negative. She was given ferrous sulphate and folic acid to supplement iron and folate levels, and given a return date of one month. She however never tuned up again to the antenatal clinic.
On 6/4/2011 she was taken to a private clinic but due to her condition, she was referred to the provincial general hospital where she came in poor condition. She started labour some hours after admission. Physical examination showed signs of pallor on conjunctiva and palms of the hands, facial and pedal pitting oedema. She also had clubbing of finger nails. She had laboured breathing, chest recession and bilateral crepitations on auscultation. A repeat haemoglobin level estimation gave a result of 2g/dl. Blood for grouping and cross match was taken and the obstetrician ordered blood transfusion of three units of packed cells if available otherwise whole blood. This was not available till in the morning at 8.30AM when two units of whole blood were availed. Since admission the patient was put on Oxygen and the head of bed raised. The bed had sidebars to prevent her from falling off. At 8.00AM a vaginal examination was done to assess the onset of labour and the cervix was found to be 7CM dilated and the membranes were bulging. Artificial rupture was done, clear liquor was drained and there was no cord prolapse. The mother was therefore anticipated for a vaginal delivery.
During transfusion vital signs observations were done half hourly with no significant deviations noted. After the first unit of blood (10.15AM) the mother’s condition was getting worse and the doctor ordered intravenous lasix 80mg stat, intravenous aminophylline 250mg slowly. Things seemed to be worsening and at 10.30AM the mother started gasping, 20 minutes after commencement of the second unit blood. Cardio-pulmonary resuscitation was instituted and the anaesthetist was called to assist but when he arrived, the mother had no cardio-pulmonary activity. He certified the death and the body was put aside for last offices.
The objectives of the study included: i. to confirm anaemia in pregnancy as a cause of maternal mortality in Coast Provincial General Hospital ii. to evaluate the management offered to antenatal mothers with anaemia in pregnancy iii. to determine the outcome of poorly managed anaemia in pregnancy
The study would offer a comparison between documented information and the case scenario.
2. Literature review Anaemia is a reduction in the oxygen carrying capacity of the blood.
Types:
The common types of anaemia that may occur in pregnancy include:
i. Anaemia of pregnancy whereby a woman’s blood volume increases by as much as 50%. This causes haemodilution but is not considered abnormal unless the levels fall too low. ii. Iron deficiency anaemia
This is the most common type of anaemia in pregnancy. During pregnancy, there is increased demand for iron, as the fetus uses the mother’s red blood cells for growth and development especially in the last three moths. Deficiency occurs if the mother did not have excess red blood cells stored in bone marrow before she conceived. The stored iron is used to help meet the baby’s needs. Deficiency in iron leads to less haemoglobin as iron is a constituent of haemoglobin
iii. Vitamin B12 deficiency
This is common in women who are strict vegetarians. Vitamin B12 is important in forming red blood cells and in protein synthesis iv. Blood loss
This could be as a result of menorrhagia and post partum haemorrhage during previous pregnancies. If a woman does not have adequate iron stores, she is unable to replace lost red blood cells, hence becomes anaemic.
v. Folic acid deficiency
Folic acid is a B-vitamin that works with iron to help with cell growth. Deficiency is often associated with iron deficiency since both folic acid and iron are found in the same types of foods. Folic acid deficiency is associated with congenital defects of the brain and spinal cord.
Signs and symptoms of anaemia
Anaemia in pregnancy may not have obvious symptoms unless the cell counts are very low. Each woman may experience symptoms differently.
They include: • Pallor on the skin, mucosal linings and nail beds • Signs of specific causes of anemia like Koilonychia (in iron deficiency), jaundice (in haemolytic anaemia) bone deformities (in thalassaemia major) or leg ulcers (in sickle cell disease) • In severe anaemia there may be signs of hyperdynamic circulation: - tachycardia, bounding pulse, flow murmurs and cardiac ventricular hypertrophy. Signs of heart failure may also be present.
Diagnosis
Anaemia is usually discovered during a prenatal examination through a routine blood test for haemoglobin or hematocrit levels. The cell size can also be measured by flow cytometry, hence distinguishing between the causes of anaemia. According to World Health Organization, a pregnant woman has anaemia when the Hb is less than 11g/dl.
Treatment
This depends on the type and severity of anaemia. Mild to moderate iron deficiency anaemia is treated by oral iron supplementation with ferrous sulphate, ferrous fumarate, or ferrous gluconate.
Taking iron supplements with orange juice is of benefit as it contains vitamin C which aids in the body’s ability to absorb iron. A rare iron replacement method is by administering parenteral iron either intramuscularly or intravenously. Vitamin supplements given orally or subcutaneously replace folic acid and vitamin B12 deficiencies respectively.
In cases of severe anemia or ongoing blood loss, a blood transfusion may be necessary especially when delivery is imminent.
Prevention • Good pre pregnancy nutrition helps prevent anaemia as well as build other nutritional stores in the mother’s body. A balanced diet during pregnancy helps maintain the levels of iron and other nutrients needed for the health of the mother and growing baby. • Administration of vitamin supplements containing 400 ug of folic acid is recommended for all mothers during pregnancy. This is because natural food sources of folate are poorly absorbed and much of the vitamin is destroyed in cooking. Good history taking during antenatal care may reveal a preexisting problem or information on lifestyle that puts the woman at the risk of anaemia. Advice and explanation which are appropriate to the particular woman can be given taking into account her health and religion and cultural preferences. • Antenatal profile to include level of haemoglobin, stool analysis and urine analysis will give suggestions of possible anaemia or risk of anaemia and correction made early by administration of iron, folate and vitamin B12 supplements, and treatment of early abnormality in stool or urine.
Associated risks of anaemia
i. Mother o Reduced enjoyment of pregnancy and motherhood owing to fatigue o Reduced resistance to infection caused by impaired cell-mediated immunity o Reduced ability to withstand postpartum haemorrhage o Potential threat to life
ii. Foetus/ Baby • Increased risk of intrauterine foetal hypoxia and growth retardation Preterm birth • Low birth weight • Increased risk of perinatal morbidity and mortality 3. Method
The selected subject was among the mothers who did not walk out of the hospital. Cases of maternal mortality have been occurring on average one mother per week at the Coast Provincial General Hospital. Anaemia in pregnancy has been the highest cause of mortality in the institution.
Zawadi had attended antenatal clinic for the first time at a gestational age of thirty weeks. Antenatal profile carried out revealed haemoglobin level of 7g/dl, an indication of anaemia. Urine and stool analysis were normal. She was offered iron and folic acid supplements, given prophylactic antimalarial treatment and dewormed. She did not attend clinic again till the date she was brought to the labour ward in poor condition at term.
On history taking, the mother was 22 years old, not educated and now had the fourth pregnancy. She came from a village where most residents are poor financially. On physical examination, the woman was restless and dyspnoeic with signs of congestive cardiac failure. The woman died before spending twenty four hours in the hospital with the baby unborn.
The study was to take into account the presence of signs and symptoms of anaemia in pregnancy in the subject, compare the antenatal profile report with the current one on admission and relate to the outcome. Any gaps in management of anaemia will also be evaluated.
The results of anaemia in pregnancy are also eminent in this study since the mother went into labour while in severe anaemia and died with the baby in utero.
4. Results
The assessment involved history taking to include name, age, residence, education level, parity and last menstrual period date so as to assess gestational age. Some of the information was obtained from the antenatal profile card. These included the blood group, and Rhesus factor, the date of first antenatal visit and investigations like Khan Test, HIV status, urine and stool analysis, haemoglobin level results and any interventions done.
The woman was from Utange area. She was 22 years old and uneducated. She was para3+0 gravida 4. Her last menstrual period was date was 20/7/2010, so the expected date of delivery was 27/4/2011. The gestation period was therefore 37 weeks on the date of admission that is 6/4/2011.
From the antenatal card the mother’s blood group was recorded as O positive, Khan test was negative, HIV test was negative. Stool and urine analysis were normal, haemoglobin level was 7g/dl and blood slide for malaria parasites was negative. These were done on the first day of antenatal clinic attendance, 15/3/2011. Any history of previous blood transfusion was also asked, and in this case the woman had never been transfused before, neither had she been admitted in hospital before. All her previous deliveries were home deliveries. She had complaints of headache, dizziness and palpitations, lasting for about one week.
Physical examination included assessing the general condition of the woman on admission. She was generally sick looking and restless. The conjunctiva and palms of hands had pallor. The mucous membranes on the lips looked cyanosed. The finger nails had clubbing. There was tachypnoea, flaring of nasal alae and chest recession on breathing. Transmission sounds and bilateral crepitations were heard on chest auscultation. There was pedal and facial oedema that was pitting.
The fundal height was 38 weeks, engagement descent was 3/5, cephalic presentation with a longitudinal lie. It was not possible to assess foetal heart state due the mother’s restlessness. On vaginal examination with help from other team members to hold down the mother, the cervix was thin, 7 cm dilated, with bulging membranes. Artificial rupture of membranes was done, obtaining clear liquor. There was no cord prolapse. The mother’s vital signs ware temperature – 36.5oC, pulse rate 70/minute, respiration 20 /minute, blood pressure 80/40mmHg. Blood for haemoglobin level, grouping and cross matching was taken. The haemoglobin level was found to be 2g/dl. Blood group was O positive but there was no blood in the blood bank. Oxygen was administered by mask 6 litres /minute.
The patient’s response was poor because at the time of admission there were already signs of heart failure and blood could not be availed immediately. The stress of labour made the mother’s condition worse. She had carried the pregnancy while still anaemic and never went back for follow-up until the day of admission. She therefore fell a victim whose life and that of her baby could not be salvaged in the institution’s set up. 5. Interventions
Interventions for managing Zawadi’s condition were instituted antenatally when the haemoglobin level was found to be low. Iron and folic acid supplements were given to be taken at home. Routine deworming and malaria prophylactic regimen was given. A return date of one month was given, but the mother never turned up. This lost contact between the health team and the mother.
During admission, the woman was put on oxygen 6 li/minute by mask. Blood for haemoglobin level, grouping and cross matching was taken. With the hemoglobin level being 2g/dl, urgent blood transfusion was required. Blood was not available so the mother was managed on oxygen, as labour was observed for progress. The mother was propped up in bed, which had sidebars to prevent her from falling off.
The consultant obstetrician was called to review the mother. He insisted on urgent blood transfusion. This was availed later and commenced at 8.30AM. During the blood transfusion, vital signs were observed, that is temperature, pulse, respiration rate and blood pressure half hourly. The first unit of blood ended at 10.15AM with no signs of blood reaction. The doctor ordered intravenous lasix 80mg, intravenous amminophylline 250mg and packed cells transfusion three units. The second unit of blood was started at 10.20AM. The patient’s condition started deteriorating. Gasping respirations and weak pulse were noted. Cardio-pulmonary resuscitation was instituted but no improvement. The anaesthetist was called to assist, but when he arrived the patient was found to be having no cardio-pulmonary activity. He certified the death.
Nursing care plan for the mother.
|Date and |Assessment data|Nursing |Expected outcome|Plan of action |rationale |intervention |evaluation |
|time | |diagnosis | | | | | |
|6/4/2011 |Patient |Altered comfort |The patient |Lie patient in bed|Lying in bed |Patient put in bed |Still restless |
|10.40PM |complains of |related to the |should be | |ensures blood |at 10.43PM | |
| |headache, |disease as |comfortable | |circulation to the | | |
| |dizziness, is |evidenced by | | |vital organs | | |
| |restless |patient’s | | |reducing the | | |
| | |complaints and | | |discomfort | | |
| | |restlessness | | | | | |
|6/4/11 |Pallor on |Impaired tissue |The haemoglobin |Administer either |Blood |Blood transfusion |Less pallor, tachypnoea |
|10.40PM |conjunctiva, Hb|oxygenation |level should be |whole blood or |administration |started at 8.30AM |still present |
| |2g/dl, |related to low |raised |packed cells |raises the |on 7/4/2011 | |
| |tachypnoea |haemoglobin |immediately | |haemoglobin level | | |
| | |level as | | |in patient’s blood | | |
| | |evidenced by | | |by providing | | |
| | |pallor and | | |healthy red blood | | |
| | |tachypnoea | | |cells. This | | |
| | | | | |improves Oxygen | | |
| | | | | |carrying capacity | | |
|6/4/11 |Flaring of |Impaired gaseous|The gaseous |Administer Oxygen,|Oxygen |Patient put in bed | |
|10.40PM |nasal alae, |exchange related|exchange should |elevate end of bed|administration |and propped up at | |
| |chest |to disease |be improved | |increases the |10.43PM, Oxygen | |
| |recession, |process as | | |concentration of |administered | |
| |transmitted |evidenced by | | |Oxygen in the air |through mask at 6 | |
| |sounds and |flaring nasal | | |inhaled, elevating |li/min | |
| |crepitations |alae and chest | | |end of bed reduces | | |
| | |recession, | | |pressure of | | |
| | |transmitted | | |abdominal organs on| | |
| | |sounds and | | |the lungs and heart| | |
| | |crepitations | | |hence improve lung | | |
| | | | | |expansion and | | |
| | | | | |cardiac activity | | |
| | | | | |respectively | | |
|6/4/11 |Patient has |Impaired tissue |The oedema |Administration of |Diuretics act on |Lasix given as | |
|10.40PM |facial and |perfusion |should subside |diuretics |the kidney tubules |prescribed 80mg | |
| |pedal oedema |related to | | |to reduce water |intravenously | |
| | |excess | | |reabsorption hence | | |
| | |intercellular | | |increase removal of| | |
| | |fluid as | | |water through urine| | |
| | |evidenced by | | | | | |
| | |oedema | | | | | |
|7/4/11 |Patient on |Risk for blood |Patient should |Observe vital |Alteration of vital|Vital signs |No signs of blood |
|8.30AM |blood |reaction related|have no blood |signs before |signs during |recorded before |reaction at the end of |
| |transfusion |to introduction |reaction |transfusion and |transfusion may |transfusion and |transfusion(10.15AM) |
| | |of foreign blood| |during |give an indication |half hourly | |
| | | | |transfusion, |of a possible blood|thereafter, | |
| | | | |countercheck the |reaction, |counterchecking | |
| | | | |blood record and |counterchecking the|done by the medical| |
| | | | |patient’s details |blood and patient’s|officer on duty and| |
| | | | |by two staff |details by two |the nurse who | |
| | | | |members |staff will ensure |commenced the blood| |
| | | | | |that the right |transfusion | |
| | | | | |blood is given to | | |
| | | | | |the right patient | | |
|7/4/11 |Patient in |Risk for |prevent foetal |Administration of |Oxygen |Patient started on | |
|8.00AM |labour, VE |intrauterine |hypoxia and |Oxygen, artificial|administration |Oxygen by mask at | |
| |cervix 7CM |foetal hypoxia |hasten delivery |rupture of |increases the |10.43PM, artificial| |
| |dilated, is |and maternal |vaginally |membranes, blood |concentration of |rupture of | |
| |restless, Hb |distress related| |trandfusion |Oxygen the mother |membranes done at | |
| |2g/dl |to mother’s poor| | |breaths in hence |8.05AM, blood | |
| | |condition as | | |the foetus, |transfusion started| |
| | |evidenced by | | |artificial rupture |at 8.30AM | |
| | |active labour | | |of membranes | | |
| | |and low Hb in a | | |increases the rate | | |
| | |restless mother | | |of cervical | | |
| | | | | |dilatation, blood | | |
| | | | | |transfusion | | |
| | | | | |provides healthy | | |
| | | | | |red blood cells to | | |
| | | | | |improve Oxygen | | |
| | | | | |carrying capacity | | |
6. Conclusion. The case study displays a picture of one of the causes of maternal morbidity and mortality in the Coast province. The subject in this case comes from an area where most of the residents are of poor standards of living. This suggests that food availability is an issue. The area is dry and farming is only practiced during the rainy season so fresh green vegetables are locally available only during this time. With both the woman and her husband being unemployed, buying the required amount and quality of food seems to have been unaffordable. Another concern goes to the management of antenatal mothers who are found to have anaemia. In this case Zawadi was found to be having haemoglobin level of 7g/dl at 30 weeks gestation. In addition to whatever drugs she was given, a follow up through home visit would have probably helped in ensuring her response. She had a history of home deliveries in all her previous pregnancies, and noting the gestation period at which she started attending antenatal clinic, some degree of ignorance should have been suspected. The mother should therefore have been handled such that education on anaemia in pregnancy should have been given and the importance of monitoring be emphasized. Failure to follow the mother aggressively ended up with the anaemia getting worse, as seen on admission that the mother came in severe anaemia in labour. She could neither withstand labour nor caesarian section and the end result was death of the mother with her unborn baby. The management of the mother since admission started well with taking her health history and doing physical examination. The antenatal visit Haemoglobin level necessitated for a check Hb but despite finding it to be too low, there was no blood available to raise it immediately. It took about ten hours to get blood for transfusion. This might have contributed to the deterioration of the mother’s condition. The fact that the patient died after getting one unit of blood suggests that the blood was availed when it was too late to reverse the damage already done, for example congestive cardiac failure. The congestive cardiac failure may also have been aggrevated by the blood transfusion due to increase in circulatory volume. This necessitated the need to administer packed cells rather than whole blood but this was unavailable hence putting the patient at greater risk of cardiac overload. The health industry should ensure that the follow up of women with anaemia in pregnancy be taken seriously. This can be done through door to door family nursing to identify the mothers at risk or those already with the problem. Those seen at the health facilities should be given health education on nutrition and the dangers of anaemia in pregnancy be made known to the mothers. They should be managed as individuals so that their level of understanding, level of anaemia and gestation should guide in their management. Those who do not turn up for follow up should be traced and encouraged to take care of their health. Admission of such mothers may be necessary so that they receive the supplements under direct observation. If not able to tolerate the oral iron supplements parenteral ones should be administered. Correction of anaemia in pregnancy should be ensured before the onset of labour so that the mother is able to endure the stress of labour. This will reduce the chances of having intrauterine foetal hypoxia and maternal distress which lead to intrauterine foetal death and maternal death.
REFERENCES 1. Bennet V. R, Brown L. K. (1999). Myles Textbook for midwives 13th edition. Churchill Livingstone. New York. 2. Anaemia. Available at htt://en.wikipedia.org 3. Anaemia in pregnancy. Available at htt://www.chkd.org
ROSE NJERI WANGARI MBOGO
References: 1. Bennet V. R, Brown L. K. (1999). Myles Textbook for midwives 13th edition. Churchill Livingstone. New York. 2. Anaemia. Available at htt://en.wikipedia.org 3. Anaemia in pregnancy. Available at htt://www.chkd.org ROSE NJERI WANGARI MBOGO
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