HYPOGLYCAEMIA

 This is a metabolic disorder in which the blood glucose

level falls below 2.6 mmol/L. At term, the baby’s glucose
level is almost equal to that of the mother but gradually
drops within 3-4 hrs after birth. This is why the baby has
to be fed within four hours of life. The baby’s maintain
their energy requirements as long as they are kept warm.
 This condition is common in infants of diabetic mothers.
 Due to excess glucose, the large babies (macrosomia). At
birth the glucose level falls rapidly while insulin levels re-
main relatively high so the baby is at risk of hypoglycemia
.this is why such babies are admitted to the NBU.
 Prolonged hypoglycaemia can lead to mental retardation,
permanent neurological damage and death due to respira-
tory and metabolic acidosis.

PREDISPOSING FACTORS
 Low birth weight
  Prematurity
 Birth injuries
 Maternal diabetes mellitus
 Asphyxia
 Septicaemia
 Respiratory distress syndrome

CLINICAL FEATURES
 Low blood glucose less than 2.6 mmol/L
 Poor feeding
 High pitched cry
 Lethargy
 Irritability
 Hypotonic muscle activity
 Hypothermia
 Apnoea

NURSING MAMAGEMENT
  Give 10% dextrose infusion until normal glucose levels
are achieved.
 Encourage the mother to breastfeed the baby
 Feed through NGtube or cup and spoon expressed
breast milk.
 If the hypoglycemia is severe, put up 10% dextrose infu-
sion and give 65-85 mls/kg of body weight in 24hrs.
 Give bolus dose of 25% dextrose 2wmls/kg body
weightiv slowly for 30 min.
 Closely monitor the glucose levels 1 hourly until the
general condition is stable or normal levels have been
achieved.
 Once the normal levels have been achieved, wean off
the dextrose and observe closely for changes in the con-
dition.

PREVENTION
 Taking blood glucose levels at birth and introducing glu-
 cose feeds e.g. dextrose or breastfeeding within 1hr of
life.
 Prevent hypothermia.
 Monitoring glucose level 2hrly for the first 6-8 hours.
 Infants of diabetic mothers should be admitted into NBU
and blood glucose level regularly checked.

COMPLICATION
 Hypothermia
 Convulsions
 Brain damage
 Neonatal death as an outcome.

NEONATAL HYPOTHERMIA
 This is a condition in which the neonates body tempera-
ture falls below 36*C .the baby losses heat through ra-
diation,conduction, convection and evaporation.
PREDISPOSING FACTORS
 Prematurity
 Asphyxia neonatorum
 Maternal diabetes mellitus
 Respiratory distress syndrome
 Cold environment

CLINICAL FEATURES
 Rectal temperatures is below 36*C
 Baby feels cold on touch
 Paleness of extremeties and face
 Very weak cry
 Low respiration rate
 Baby not eager to feed (poor feeding)

NURSING MANAGEMENT
 Nurse the baby in a warm environment in a resuscitaire
or wrap it in warm clothings
  Feed the baby with expressed breast milk via NG tube
 Give the baby extra glucose e.g. dextrose
 Closely observe the baby for signs of hypoglycaemia and
if present, give 10% dextrose
 Check for and treat convulsions with anticonvulsants

PREVENTION
 Delivery should be conducted in a room temperature
 Put the baby on resuscitaire or in incubator to compen-
sate heat loss to the environment.
 Baby should not be bathed within 1hr of life but top-
tailing can be done after one hour.
 Encourage skin to skin contact (kangaroo method) when
carrying the baby.

COMPLICATIONS
 Convulsions
 Hypoglycaemia
  Brain damage

HAEMORRHAGES
Haemorrhages may be due to:
 Trauma
 Disruptions in blood flow or can be related to:
 Coagulopathies
 Other causes.

HAEMORRHAGES DUE TO TRAUMA

A. Cephalhaematoma
 It is an effusion of blood under the periosteum that covers
the skull bones.
Causes
 friction between the fetal skull and maternal pelvic bones,
e.g in cephalopelvic disproportion or precipitate labour -
 the periosteum may be torn from the bone, causing bleed-
ing underneath.
 Cephalhaematomas may also occur during vacuum-
assisted births.

Clinical picture
 Unlike caput succedaneum, a cephalhaematoma is not
present at birth; the swelling appears after 12 hours,
grows larger over subsequent days and can persist for
weeks.
 The swelling is firm, does not pit on pressure, does not
cross a suture and is fixed

Management
 No treatment is necessary and the swelling subsides when
the blood is reabsorbed.

B. Subaponeurotic haemorrhage
 The epicranial aponeurosis, is a sheet of fibrous tissue
that covers the cranial vault allowing for muscles to at-
tach to the bone
 It provides a potential space above the periosteum
through which veins travel.
 Excessive traction on these veins results in haemorrhage,

Causes
 is more often associated with forceps and vacuum-
assisted births, and severe dystocia

Clinical picture
 The swelling is present at birth, increases in size and is a
firm, fluctuant mass.
 The scalp is movable rather than fixed.
 The swelling can cross sutures and extend into the sub-
cutaneous tissue of neck and eyelids.
 The baby may appear pale, be hypotonic, tachycardic and
 tachypnoeic and demonstrate discomfort or pain with
head movement or handling of the swelling.
Management
 If the subaponeurotic haemorrhage is excessive, there is
the potential for severe shock, disseminated intravascular
coagulation (DIC) and death.
 This emergency situation requires immediate medical as-
sistance, resuscitation, stabilization and full supportive
care, including blood trans- fusion
 With a smaller haemorrhage and in the babies who sur-
vive a larger haemorrhage, the blood is reabsorbed and
the swelling and bruising resolve over 2–3 weeks.

C. Subdural haemorrhage
 Trauma to the fetal head, such as excessive compression
or abnormal stretching, may tear the dura, particularly
the tentorium cerebelli, rupturing venous sinuses and re-
sulting in a subdural haemorrhage.
Predisposing factors
 abnormal or excessive moulding, such as in
 precipitate labour or rapid birth,
 malpositions,
 malpresentations,
 cephalopelvic disproportion, or undue compression during
forceps manoeuvres.

Management
 If the haemorrhage is excessive, there is the potential for
severe shock, DIC and death. This emergency situation
requires immediate medical assistance – resuscitation,
stabilization and full supportive care, including blood
transfusion
 A baby with a small haemorrhage may demonstrate no
signs and resolution is spontaneous.
 Supportive treatment focuses on replacing blood volume
 and controlling the consequences of asphyxia and raised
intracranial pressure.
 Surgery to relieve pressure or subdural taps or shunt
placement to drain large collections of blood may be re-
quired.
 A shunt is a drainage tube surgically inserted and con-
nected to a one-way valve placed subcutaneously behind
the ear.).

HAEMORRHAGES DUE TO DISRUPTIONS IN BLOOD

FLOW

A. Subarachnoid haemorrhage
 A primary subarachnoid haemorrhage involves bleeding
directly into the subarachnoid space.
 A secondary haemorrhage involves leakage of blood into
the subarachnoid space from an intraventricular haemor-
rhage.
Signs
 The affected baby may demonstrate no signs while others
may have generalized convulsions from the second day of
life and have apnoeic episodes.

Diagnosis
 Blood in a non-traumatic lumbar puncture may assist in
diagnosis,
 cranial USS, CT or MRI.

Management
 Supportive treatment focuses on replacing blood volume
and controlling the consequences of asphyxia and raised
intracranial pressure.
 Surgery to relieve pressure or subdural taps or shunt
placement to drain large collections of blood may be re-
quired.
B. Germinal matrix haemorrhage, intraventricular
haemorrhage and periventricular haemorrhagic infarc-
tion
Causes
 Early factors include
 obstetric haemorrhage, lack of antenatal steroids,
 low one minute Apgar score and
 low umbilical artery pH.
 Later risk factors include
 acidosis,
 hypotension,
 hypertension,
 mechanical ventilation,
 apnoea,
 rapid volume expansion,
 rapid administration of hyperosmolar solutions, pneumo-
thorax and tracheal suctioning.
Signs
 Most affected babies show no signs or signs that are non-
specific therefore the haemorrhage/infaction/lesion is de-
tectable only on USS.
 If the haemorrhage is larger the clinical features include
 apnoeic episodes that become more frequent and severe,
bradycardia, pallor, falling packed cell volume,
 tense anterior fontanelle,
 metabolic acidosis and convulsions.
 The baby may be limp or unresponsive.

Management
 Prevention of hypoxic events and blood flow and pressure
fluctuations is essential.
 Care is focused on maintaining normothermia, normogly-
caemia, oxygenation and comfort.

HAEMORRHAGES RELATED TO COAGULOPATHIES

HAEMORRHAGIC DISEASE OF THE NEWBORN [VITAMIN
K DEFICIENCY BLEEDING]
 This bleeding occurs during the first few days of life due
to vitamin K deficiency. Vitamin K is synthesized by the
bowel normal flora and its role is to convert clotting fac-
tors such as prothombin, thrombokinase, thromboplastin.
 To prevent HDN the neonates are given vitamin K 0.5-1
mgi.m.

predisposing factors
 Hereditary factors- clotting factor defect e.g. haemophilia
 Prematurity
 Birth trauma
 Treatment with antibiotics
 Respiratory distress syndrome
 Disseminated intravascular coagulopathy (DIC)
  Birth asphyxia
 Mothers who are on drug such as warfarin, heparin and
Phenobarbital

Clinical features
 Continuous oozing of blood from the umbilical cord
 There is a spontaneous bleeding from various parts of
the body
 Bleeding in the mucous membrane of GIT and may pre-
sent with maleana stool or haematemesis
 Continuous bleeding from any punctured blood vessel or
injection site thus when looking for venous access avoid
puncturing femoral or jugular veins which are the larg-
est veins in the body
 Haematuria or omphalorrhagia

Nursing management
 Upon admission into NBU, administer vitamin K 0.5-1 mg
i.m
 Preserve all linen soiled by blood for estimination of blood
loss
 Administer vitamin K 1-2 mg to arrest bleeding immedi-
ately
 Observe vital signs TPR ¼ hrly
 If bleeding is severe, transfuse fresh blood or frozen plas-
ma at 20mls/kg of body weight
 Obnserve for signs of shock and if present transfuse with
packed cells and fresh whole blood at 75 -100mls/kg of
body weight if the baby is term
 General management is like any other baby in the unit

Complications
 Anaemia
 Hypovolaemic shock
  Brain damage

Thrombocytopenia
 Thrombocytopenia results from a decreased rate of for-
mation of platelets or an increased rate of consumption
and is defined as a platelet count of less than 150 ×109/l,
and severe thrombocytopenia is a platelet count of less
than 50 ×109/l
Fetal causes include
 alloimmunity,
 congenital infection and trisomies.
 Early onset (less than 72 hours) neonatal causes include:
 placental insufficiency,
 perinatal asphyxia,
 perinatal infection,
 DIC and alloimmunity.
 Late onset (after 72 hours) neonatal causes include late
onset sepsis, necrotizing enterocolitis, congenital infection
 and autoimmunity.

Diagnosis
 It is based on history, clinical examination and a reduced
platelet count.

Management
 Mild or moderate thrombocytopenia is usually self-
limiting and requires no treatment.
 In severe cases, the treatment usually includes platelet
concentrate transfusion/s, although the optimum regime
is yet to be determined.

Disseminated intravascular coagulation (consumptive

coagulopathy)
 Is an acquired coagulation disorder associated with the
release of thromboplastin from damaged tissue, stimulat-
ing abnormal coagulation in the microcirculation as well
 as excess fibrinolysis.
 Maternal causes of neonatal DIC include pre-eclampsia,
 eclampsia and placental abruption.
Fetal causes include:
 severe fetal compromise,
 the presence of a dead twin in the uterus and traumatic
birth.
 Neonatal causes include conditions resulting in hypoxia
and acidosis,
 severe infections,
 hypothermia,
 hypotension and thrombocytopenia

Diagnosis
 Is made from clinical signs and laboratory findings that
show a low platelet count, low fibrinogen level, distorted
and fragmented red blood cells,
 low haemoglobin and raised fibrin degradation
Treatment
 Must focus on correction of the underlying cause if possi-
ble and full supportive care will be required.
 Control of DIC requires transfusions of fresh frozen plas-
ma, concentrated clotting factors and platelets. .
 If anaemia is diagnosed, transfusions of whole blood or
red cell concentrate are required.
 Occasionally an exchange transfusion of fresh heparinized
blood may be performed, to remove fibrin degradation
products FDPs while replacing the clotting factors.

HAEMORRHAGES RELATED TO OTHER CAUSES

A. Umbilical haemorrhage
 This usually occurs as a result of a poorly applied cord
ligature.
 The use of plastic cord clamps has almost elimi- nated
this type of haemorrhage, although it is essential to avoid
catching or pulling the clamp.
B. Vaginal bleeding
 A small temporary vaginal discharge of bloodstained mu-
cus occurring in the first days of life, pseudomenstrua-
tion, is due to the withdrawal of maternal oestrogen.

C. Haematemesis and melaena

 These signs may present when the baby has swallowed
maternal blood during birth, or from cracked nipples dur-
ing breastfeeding. If the cause is swallowed blood, the
condition is self- limiting and requires no specific treat-
ment.

D. Haematuria Haematuria
 may be associated with coagulopathies, urinary tract in-
fections and structural abnormalities of the urinary tract.
Treatment of the primary cause should resolve the hae-
maturia
E. Bleeding associated with intravascular access
 Some sick or preterm babies require the insertion of cath-
eters, lines or cannulae into central or peripheral arteries
or veins, or both, to provide routes for blood sampling,
blood pressure monitoring or the infusion of fluids and
drugs.
 Skilled technique, close observation and careful handling
of babies with intravascular access are imperative to pre-
vent potentially fatal haemorrhage.