Interesting Peds ED Case

HPI: Pt is a 4 yo black male brought to the ED by his father. Father stated that the pt was in his usual
state of good health until about 24 hours prior to his arrival in the ED. On the day prior dad says that
the child started to have “fevers in the 90’s” and extreme drowsiness. He says that the child slept all day
the previous day, all night and most of the day prior to arriving in the ED. Father says that he gave the
child 1 adult motrin tablet this morning around 7 am this morning which the child was able to swallow
but no other medications. When asked, dad says that the child did have a little congestion and a runny
nose once earlier in the day. The child had also c/o a stomach ache and head ache. Dad noted a poor
appetite but denied any nausea, vomiting or diarrhea. When asked about past medical history, dad
explained that he thought the child had been treated for malaria about 1 month ago. He had no idea of
the type of malaria or what medication the pt had taken or for how long. The story unfolded that the
child was born in Kenya and had lived there until his dad traveled to Kenya and brought the child back to
the US on December 30th. Dad says that as far as he knows, the child has had all of the required
vaccinations. He does say that the child is in daycare here.

Physical Exam
BP 102/65 | Pulse 136 | Temp(Src) 98.2 °F (36.8 °C) (Oral) | Resp 23 | Wt 16.4 kg (36 lb 2.5 oz) | SpO2
100%
Constitutional: He appears well-developed and well-nourished. No distress. Pt is sitting in his dad’s
lap asleep
Head/Ears:Atraumatic. Tympanic membranes normal bilaterally.
Nose: Nose normal, no drainage.
Mouth/Throat: Mucous membranes are moist. Dentition is normal. Oropharynx is clear.
Eyes: Conjunctivae are mildly icteric. Pupils are equal, round, and reactive to light.
Neck: Normal range of motion. Neck supple.
Cardiovascular: Pt is mildly tachycardic but regular rate and rhythm.
Abdominal: Soft. Bowel sounds are normal. No apparent tenderness, guarding or rebound.
Musculoskeletal: Normal range of motion.
Neurological: Pt is quite somnolent, easily awoken, appropriate but falls back to sleep
Skin: Skin is warm and dry. Capillary refill takes less than 3 seconds.

His labs were as noted below:

MALARIA SMEAR
Result Value Range
MALARIA SMEAR PRESENT (*) ABSENT
PATHOLOGIST COMMENT P. FALCIPARUM

BASIC METABOLIC PANEL (7)

Result Value Range
Sodium,S 128 (*) 136 - 145 mmol/L
Potassium 4.1 3.5 - 5.1 mmol/L
Chloride 97 95 - 110 mmol/L
Co2 23 (*) 24 - 32 mmol/L
Glucose 107 (*) 70 - 99 mg/dL
BUN 13 7 - 21 mg/dL
CREATININE,S 0.43 (*) 0.64 - 1.27 mg/dL
ANION GAP 12 8 - 14
CALCIUM,TOTAL 8.9 8.4 - 10.2 mg/dL

CBC WITH DIFFERENTIAL

Result Value Range
WBC COUNT 3.8 (*) 4.0 - 12.0 10E9/L
RBC Count 3.65 (*) 4.10 - 5.30 10E12/L
HGB 10.2 (*) 11.0 - 14.5 g/dL
Hematocrit 29 (*) 33 - 43 %
MCV 78 74 - 89 fL
MCH 28 24 - 30 pg
MCHC 36 32 - 36 g/dL
RDW 15.0 (*) 12.0 - 14.0 %
PLATELET 54 (*) 150 - 450 10E9/L
MPV 8.9 (*) REFERENCE RANGE
NOT ESTABLISHED fL
% Immature Granulocytes 0 0-2%
% NEUTROPHILS 51 15 - 55 %
% Lymphs 46 41 - 77 %
% Monos 1 1 - 12 %
% EOS 1 0-6%
% BASOS 1 0-2%

ANISOCYTOSIS 2+
HYPOCHROMIA 1+
MICROCYTOSIS 2+
POLYCHROMASIA 1+

LACTIC ACID ASSAY

Result Value Range
LACTIC ACID 3.4 (*) 0.5 - 2.2 mmol/L
POCT INFLUENZA A/B
Result Value Range
Rapid Influenza A Ag Negative Negative
Rapid Influenza B Ag Negative Negative

Here is a quick review of Malaria for your reading pleasure.

The malaria parasite life cycle involves 2 hosts. When a female Anopheles misquito bites a human, she
inoculates sporozites into the human host. These little suckers infect liver cells and mature into
schizonts which rupture and release merozoites. ( This is starting to sound like a horror movie!) The
merozoites invade the red blood cells and undergo asexual multiplication in the RBCs o/w known as
erythrocytic schizogony . (Can’t make this stuff up). In the blood, successive broods of parasites grow
inside the red cells and destroy them. More merozoites are released and continue the cycle by invading
other red blood cells. It’s these blood stage parasites that cause the symptoms of malaria. Certain
forms of blood stage parasites are called gametocytes. The gametocytes come in a guy form
(microgametocytes) and a gal form (macrogametocyte). The mosquito eats them and while in the
mosquito’s stomach the microgamete penetrates the macrogamete and they generate zygotes. The
zygotes invade the midgut wall of the mosquito, turn into oocysts. The oocyts grow, rupture and spew
out sporozoites. The sporozoites make their way to the mosquito’s salivary gland where they hang out
and wait for the wild ride to another human liver. Go back to the beginning of this paragraph because
the cycle has just started again. It’s easy to see why the Noble Prize in Physiology or Medicine was
awarded at least 4 times for work associated with Malaria.

Approximately 1,500 cases of Malaria are diagnosed in the US each year. Of the 4 Plasmodium species
that infect humans, falciparum is the one that can rapidly progress to severe illness or death. Be
especially mindful of travel history to sub-Saharan Africa, Hispaniola and Papua New Guinea. Incubation
period for Falciparum is 7-18 days. The work up for Malaria is relatively simple per the CDC Malaria
Hotline MD who is available to you 24/7 at (770)488-7788. It includes a CBC,BMP and a thick and thin
smear all of which are available in our lab. (A positive malaria smear will get you all kinds of phone calls
from the lab including treatment advice from the pathologist.) Please note that one negative thick and
thin smear does not completely rule out malaria. If the initial smears are negative, the pt must return
for 2 additional smears done at 12-24 hour intervals.

Falciparum presents as a continuum of disease and treatment is dictated by the severity of the disease.
Uncomplicated disease consists of symptomatic illness with less than 5% parasitemia (percentage of
infected red cells on a thin smear) without evidence of vital organ dysfunction. Treatment in these cases
is oral therapy with a combination of 2 agents. Manifestations of severe Malaria include:

Impaired consciousness/coma
Prostration
Respiratory distress (acidotic breathing)
Multiple convulsions
Circulatory shock
Pulmonary edema
Acute respiratory distress syndrome
Abnormal bleeding
Jaundice
Severe anemia
Acute renal failure
Disseminated intravascular
coagulation
Acidosis
Hemoglobinuria
Parasitemia >5%
Nonspecific laboratory findings include thrombocytopenia, neutorpenia, and signs of hemolysis
including eleveated bilirubin levels and anemia. Treatment for severe malaria includes Doxycycline,
Tetracycline or Clindamycin as well as Quinidine gluconoate all of which are available in our pharmacy.
My patient got 10 mg/kg loading dose of IV clindamycin which we had easy access to while we were
waiting on the pharmacy to prepare the loading dose of quinidine gluconate. We had the loading dose
of Quinidine gluconate (6.25 mg base/kg =10 mg salt/kg) to be infused over 1-2 hours ready to go when
the transport team arrived so we didn’t start it in our ED He got the loading dose at Egleston followed
by an infusion of Quinidine gluconate in the PICU. Please note that quinidine administration puts the
patient at risk for blood pressure issues, hypoglycemia, widening of the QRS complex and prolonged QTc
interval so they have to be monitored very closely.

In the PICU at Egleston the pt was continued on the clindamycin and a quinidine gluconate drip. My
patient had 10% of his RBCs infected on our smear at Kennestone @ 1150 am which classified his case as
severe. His infectivity peaked at 33.25% at 11 pm that evening. He remained clinically stable and was
continued on the quinidine drip in the PICU until his infectivity rate was less than 1%. At that point the
pt was moved to the floor and continued on oral medications. His infectivity rate was documented as 0%
at 7 am 5 days later.