deficiency in the coagulation factors that make up the prothrombin complex (II, VII, IX,

and X), which are highly dependent on the presence of vitamin K in carrying out their

functions (Pantiyasa, 2011). Some studies suggest that this disorder is caused by vitamin

Late Onset Acquired Prothrombin Complex Deficiency (APCD) in a 27 Days Old Infant:

a Rare Case Report 983

K deficiency in infancy, but vitamin K supplementation alone cannot solve the problem

(Bhanchet et al., 1977).

Most cases that are brought to the hospital are caused by spontaneous bleeding that

occurs in the early stages of life, which is less than three months of age (Koojaroenprasit,

2012). It is very rare for the parents to check neonates' complaints at the earliest possible

condition which results in the treatment given to the patient being a little late and

worsening the patient's prognosis (Gunawan & YOESTINI, 2011).

This case report will report the incidence of late onset APCD to increase awareness

when there are early symptoms that appear in patients even though the symptoms seem

vague. So that treatment can be given as early as possible before more massive bleeding

occurs (Bruck, 1992) (Fristadi & Bharata, 2015) (Scholes, 1998).

A 27-days-old neonatus looked hypoactive was taken by his parents to the hospital

because decreased of consciousness, and his body was bluish since 1 hour ago after

antibiotics, anticonvulsants, anti-tuberculosis drugs, or anticoagulants. After delivery, the

baby was quite good, there was no history of jaundice, head trauma, or previous excessive

swinging. The patient was given breast milk and sometimes given formula milk. The

history of postnatal vitamin K injection is unknown.

Physical examination showed the baby looked pale and somnolent with the

Children Coma Scale (CSS) 7 (E1M4V2). Examination of vital signs showed the pulse

rate was 158 beats / minute (sufficient, strong, and regular filling), an irregular breath rate

of 10 times / minute, and the body temperature was 36.8 ° C. The neonatal weight was

2.5 kilograms and the birth weight now was 2.6 kilograms. The baby’s head looks

normal, with isochore pupils 3mm and 3mm, and the mouth looks bluish with the suction

(leukocytes 4.1x1000 /uL) but there is a thrombocytopenia (70,000 cells / mm3), with

blood glucose (102 mg/dL) and electrolytes (Sodium 133 mmol/L, Potassium 4.7

mmol/L, and Chloride 98 mmol/L) within normal limits and a slight increase in calcium

at a lab value of 10.3 mg/dL.

Blood gas analysis showed a respiratory alkalosis with a pH of 7.59 pCO2 18

mmHg, 141 mmHg pO2 dg base excess -2.2 mmol/L, hco3- 17.3 mmol/L.

On the hemostatic status examination, it was found that normal prothrombin time

(PT) (13 seconds) but the activated partial thromboplastin time (aPTT) was extended by

984 http://eduvest.greenvest.co.id

63 seconds. Head ultrasound imaging shows there is a bleeding on appointed from the

picture below.

30cc / 2tpm, ranitidine 2x3 mg, ampisulbactam2x150mg, phenytoin 60mg if seizures (+)

midazolam inj 0.1-0.4 mg / kg / hour. 2x3 mg furosemide injection. Pro furosemide 1.5

mg post cg 0.2 cc. The patient also was given 3meqdrip natrium bicarbonate correction,

dobutamine 5meq / kg / hr, miloz 0.1-0.4mg / kg / hr. The patient was observed in the

neonatal room and a CT scan is planned if the patient has been stable condition.

RESEARCH METHOD

This study uses a qualitative method with the type of case report. The sampling

technique used in this study the author uses the Random Sampling technique or by using

consciousness. Initial suspicion needs to be explored, especially the patient's body and

lips become bluish in color and occasionally do not breathe. The age of our patient is still

age of onset of 40 days although it can be longer than that up to three months. Most of the

complaints of APCD patients when they first come to the hospital are seizures, coma,

drowsiness, or the presence of focal neurological abnormalities. These symptoms arise

due to the process of abnormalities that occur in the intracranial so that it can cause an

increase in intracranial pressure and affect consciousness and breathing (Wahab, 2020)

(Bhanchet-Israngkura & Kashemsant, 1975).

Our patients have been breastfed since birth and occasionally get formula milk. A

study showed that babies who only consumed breastmilk had a higher risk of developing

APCD compared to babies who were alternated with formula or formula alone. Although

Late Onset Acquired Prothrombin Complex Deficiency (APCD) in a 27 Days Old Infant:

a Rare Case Report 985

barrier so it is found in breast milk at low concentrations (Gretz & Basuroy, 2013). In

infants who do not have abnormalities in their coagulation conditions, consumption of

color can be one of the manifestations of APCD on the skin, the emergence of purpura

which can be an early sign of APCD symptoms. Although often overlooked, purpura is an

early sign before the appearance of more severe symptoms such as intracranial

hemorrhage or GI tract bleeding. In one study purpura was found in 32% of patients with

APCD, even though purpura was not found even though bleeding at other sites persisted.

GI tract and intracranial hemorrhage are dangerous complications in infants born

with coagulation disorders. The mortality in both cases is quite high, even if the patient

survives, he or she will experience an accompanying disability for the rest of his life

(Pitriyani, Noch, & AK, 2019) (Wahab, 2020). Somnolence appearance of the patient

shows that the problems that occur are not only local, but there have been problems in the

intracranial that cause decreased consciousness. In addition, the apneic period can be a

studies, APCD was not associated with a decrease in platelets, so the findings in this case

were unique (Sipayung, Pakpahan, Widiyani, & Devi, 2019). One of the possible

processes that cause a decrease in platelets in our patient is the possibility of consumptive

coagulopathy that occurs in the intracranial as a form of compensation for the bleeding

that occurs. In locations that occurs bleeding, many platelets recruited to carry out

hemostasis which causes platelets in the peripheral veins to decrease (Krismen, 2014).

In our case we had a normal PT result and a prolonged aPTT. Although in many

studies related to APCD, PT and aPTT are found to be prolonged, but it is necessary to

carry out a more in-depth evaluation of what factors are experiencing the disorder.

Because only looking at PT and aPTT alone could not assess the abnormality of the

has stabilized.

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Late Onset Acquired Prothrombin Complex Deficiency (APCD) in a 27 Days Old Infant:

a Rare Case Report 987