Caso clínico.

Menina, 8 anos, há 5 dias com febre continua. Hoje ficou “doente” com episódios de
vómitos, dor abdominal, e não urinou nas últimas 12 horas. O irmão de 6 anos também
está febril há 7 dias

EO no SU

Consciente mas ligeiramente confusa. FR de 46/ min. FC 148 TA 100/80mmHg

Pulso filiforme e TRC de 4 a 5 “.
Alguma petéquias na fossa antecubital. GCS = 14/15 (O4, M6, V4). Algo agitada e
confusa.

Atitude:
Oxigénio em mascara a 15 l/min.
Acesso venoso - 18G
Análises – Hemograma, (Hmt), iono, glucose, hemocultura, F renal e hepática.

Bólus de NaCL 0,9% 300 ml em 20 min.

TRC baixou para 3 -4”, FC 135 (ainda algo elevada),

Repetiu novo bolus e a FC baixou para 120. Com TRC de 2” e ficando menos agitada.

Admitida na UCIP. Concordam?

AP: saudável sem medicações, Sem alergias conhecidas, Acordada mas ligeiramente
confusa e agitada. Com O2 em mascara, taquipneica a 40/min.
MV claro e simétrico SpO2 98%, FC 140/min sem sopros e/ou galope, TA 100/80
TRC = 4 sec. Rash petequial, 37ºC
Peso:30 kg

Hb 16.8 g dl, PCV 0.62, Plaq 80 × 109 l, Leuc 3.8 × 109 l, Na+ 134 mmol l, K+ 4.1 mmol l,
Urea 13.2 mmol l, Creatinine 117 μmol l, Glicemia 5.8 mmol l, pH 7.18, pCO2 23 mmHg,
HCO3 − 16.5 mmol l, BE −8

Diagnóstico: Dengue

Cálculo dos soros para as próximas 24 hs:

Manutenção 1700 ml = 70 ml/h

Dx 5% em NaCl 0,9% ou Dx 5% em NaCl 0,9%

Juntou 40mmol l de potassio logo que urinou.

Antibiotico?

Análise de novo:
Hb 15.4 g dl, PCV 0.55, plaq 76 × 109 l, Leuc 5.7 × 109 l, glucose 7 mmol l,
 Na 135 mmol l, K 4.3mmol l.

Será que os soros só de manutenção seriam suficiente? Hg de 16,8 e 15,4 não

significariam já hemoconcentração por fuga capilar?
Ter diminuído o Hmt para 40% teria sido mais aconselhado…

1h

Estável com 100/90 mmHg, FC 108 b min TRC 2–3”

Monitorizaçao pulso e TA de 1/1 h

Planeada monitorização analítica de 6/6 h

Às 6 h.
TA estável entre 110/90mmHg e 100/80mmHg.
Com aumento gradual da FC 95 até 138 b min entre a 4 e 6 h.

Durante as coheitas estava mais sonolenta com dificulade em acordar

FC 155 min com TRC de 4–5 sec. Pulso filiforme e TA sist 80mmHg.

Sem palidez conjuntival.

Atitude:

Repetiu bolus de 600 ml SF rápido

No local da colheita ficou um grande hematoma.

HB 17.0 g dl, PCV 0.68, plaquetas 12 × 109 l, Leuc 4.2 × 109 l, Na 131mmol l, K
5.6mmol l, pH 7.1 pCO2 35mmHg, HCO3 8.3, BE −20, lactato 2.8mmol l.

ÀS 12 h
GCS 9/12 (O2, M 4, V 3), Fc 160 min, TRC 4 sec, TA 90/43mmHg. Taquipneico a 50
min. MV assimétrico com diminuição em todo o pulmão dtº .

Atitude:
Rx tórax – derrame pleural extenso.
Gasimetria: pH7.12, HCO3 10.2 mmol l, BE −16, lactato 3.9 mmol l.
Lab das 6 h: Hg 12.8 g dl, PCV 0.47, Plaq 13 × 109 l,

Em estado de choque apesar dos aportes, há uma queda abrupta da Hg

levantando a suspeita de Hemorragia abundante não visível (GI?)

Atitude:
SNG – mostrou 150 ml de conteúdo gástrico com sangue vivo.
Atitude:
CE 300ml de CE (Sangue total??)

TA melhorou para 100/80mmHg.

Como se mantinha em choque e encefalopatica foi decidida a entubação e aventilação.

E foi decidida a inserção de CVC.

Condoradam? Que fariam?

Entubada com TET c/ cuff 6.0 cuffed

Com ketamine 2mg kg, atropine 0.02 mg kg, midazolam 0.1 mg kg e atracurium
1 mg kg.
Ventilada como:
ΔPIP 14 cmH2O, PEEP 6 cmH2O, a 30 min, Ti 0.8 sec, FiO2 0.35.

TA caiu para 88/55mm Hg.

Colocou CVC 7.0 F triplo lumen na femural vein.

Seria importante CVarterial?

Atitude:
500 ml de CE.

TA melhorou para 100/45mm Hg, mas a periferia mantinha-se fria e não havia urina.

Lab: Hb 9.8 g/dl, PCV 0.30, platelets 22 × 109 l, pH7.28 HCO3 17 mmol l, BE −3, lactate
2.8mmol l, TP 26”, apTT 135 s, controlo 36 s, D-dimero positivo, ureia 19.6mmol l,
creatinine 183 μmol l.

Atitude: Coagulopatia significativa com CID. E trombocitopenia.

Fez

PFC 400 ml em 4 hs e 4 u crioprecipitado.

Às 18 h.

90/45mm Hg taquicardia, apesar das transfusões massivas de cristalóides e derivados

do sangue. Com dificuldade em perceber se o choque estava ralacionada com a perda
hematica ou com a permeabilidade vascular.

Ecografia – boa função cardíaca, (fracção de ejecção 77%, fracção de encurtamento

45%, LVIDd 3.5 cm, LVPWs 1.9 cm).

Dado o volume de aportes sem melhoria da TA decidiu-se iniciar:

 O que iniciariam ou já deviam ter iniciado?

Dopamina 5 mcg kg min.

Manter Hematócrito ente 38 e 40%

O Hmt é fundamental ms nestes doentes pode ser enganador, Onde começa a

hemoconcentração e a fuga capilar e onde começa a hemodiluição por excesso de
aportes?

Às 24

BH: 5500 ml/24 h. Plasma freco congelado, plaquetas, sangue, cristalóides.

Diurese é de 1,2 ml/kg/h

Abdomen distendido e compliance pulmonar agravou-se com VC inferior a 6 ml/kg.

PaO2 60 a 65 mm Hg (PaO2/FiO2 150)
Ajuste de Parametros PIP 20 cmH2O e PEEP 14 cmH2O e FiO2 0.55.

Edemaciada, TA 110/80, periferia quente com TRC 2”, FC 110 - 120

Às 36 hs

Com soro de manutenção em 1500 ml/m2/dia stava estável. Hmt em 36%. E Plaquetas
em 30 30 × 109 l

Teve uma dejecção volumosa de melenas.

BH + 300 ml em 12 h. Diurese mantém-se acima de 1 ml/kg/h.

Análises revelam :
Ureia subiu de 18,3 para 27,3 e Creatinina de 163 para 476mcmol/l

AST/ALT de 111/828 IU l até 895/5348 IU l e amónia 179 mm.

Nivel de consciência continuava deprimido mesmo após a suspensão da

sedação/analgesia.

Atitude? Justifica exame imagem do SNC? (risco de hemorragia, derrame, edema)

TAC – normal.

Edemaciada, com BH acumulado de cerca de 6 000 ml. Oligo anurica em insuficiência

renal , obnubiliada (encefalopatia renal, hepática e possível post isquemica) foi
iniciada:

HDFVVC
 Hemosol tamponado com bicarbonato (não lactato pela disfunção
hepática)
Sem anticoagulação, lavando o filtro com Flushes de SF 100 ml a cada
hora.

A extracção hídrica iniciada em 200 ml/hfoi incrementada até 700 ml/h para
BH negativos diários de cerca de 1000 a 1500 ml/dia, mantendo a estabilidade
hemodinamica.

Às 48 h

Ventilação mecânica melhorou significativamente com VC avima de 12 ml/kg e a

PIP foi reduzida gradualmente até 12 cmH2O e a PEEP até 8 cmH2O, mantendo a
melhoria da oxigenação (PaO2/FiO2 >250).

ÀS 72 h

Estável, acordada, muito menos edemaciada, hemodinamicamente estável, BH nas 24 h

neg 2500 ml, Diurese a 1,5 ml/kg/h.

Decide-se: O quê? Quanto à ventilação?

E a nutrição? Não come há 3 dias…

Como deconectar e extubar?

Iniciou NP. Seria o aconselhável?

Inicou Nutrição parentérica.

Urei e creatinina melhoraram gradualmente e CRT parou ao 7º dia.

A diurese foi aumentando gradualmente mas com uma infusão de: o quê?

furosemida a 1 mg kg h nas 48 h seguintes até que diurese subiu

subitamente até 6 ml/kg/h.

4º dia

Consciente, GCS 13/15 (O V M)

Periodos de agitação ligeira.

Foi extubada e transferida.

Introduction
Dengue is the most common and important mosquito-borne viral infection1 and can manifest
as Dengue Fever (DF), which is often a self-limiting febrile illness or less commonlydengue
hemorrhagic fever (DHF). The major pathophysiologic hallmarks that distinguish DHF from DF
and other diseases are increased vascular permeability leading to plasma leakage and
circulatory collapse (Dengue Shock Syndrome/DSS). Management involves close monitoring
and early detection of shock, with prompt and judicious use of appropriate fluids to correct
hypovolemia, yet prevent fluid overload. Blood transfusions may be indicated in patients with
refractory shock or shock in the presence of falling hematocrit.

Discussion

DEN 1, DEN 2, DEN 3, DEN 4

Primary response occurs in non-immune individuals undergoing their first dengue infection,
whilst a secondary (anamnestic) response occurs in individuals having memory cells from
previous dengue infection. Secondary infection is a risk factor for DHF, including passively
acquired antibodies in infants.3 Other risk factors include virus strain and age of the patients.4
Although DHF/DSS can occur in adults, most cases are in children <15 years, with
circumstantial evidence suggesting that certain population groups are more susceptible to
vascular leak syndrome.

Initial assessment and management

Dengue virus infection may be asymptomatic, cause undifferentiated febrile illness, dengue
fever (DF) or dengue hemorrhagic fever (DHF).5 DF is often an acute biphasic fever, with
headaches, myalgia, arthralgia, rash, and leukopenia. It is commonly benign but may
occasionally
present with atypical hemorrhage . The clinical features of DHF/DSS are rather stereotyped,
with acute onset of high (continuous) fever, haemorrhagic diathesis (most frequently on the
skin), hepatomegaly, and in some cases circulatory disturbance (in the most severe form as
shock) and should be suspected in any child from an endemic area with prolonged fever of >3
days. It is thus possible to make an early and yet accurate clinical diagnosis of DHF before the
critical stage or before shock occurs, by using the pattern of clinical presentation together with
thrombocytopenia and concurrent hemoconcentration, which represent abnormal hemostasis
and plasma leakage, respectively.
It would be prudent to admit all suspected cases of childhood dengue, as there are no
definitive risk factors that predict the development of shock or bleeding. Using degree of
thrombocytopenia as admission criteria is flawed as it is poorly predictive for the development
of DSS/bleeding.7,8 The severity of DHF can be divided into four grades (Table 17.2).
Thrombocytopenia with concurrent hemoconcentration (defined as an increase in >20%
from baseline or evidence of increased capillary permeability) differentiates Grade I and II
DHF from DF. However, this differentiation can be difficult because of variations in normal
baseline hematocrit in the pediatric population (Table 17.3).

Management of grade I and II dengue hemorrhagic fever

All cases should be admitted for monitoring. Oral intake should be encouraged and in those
who are drinking poorly intravenous fluids at maintenance rates of 4–5ml kg−1 per h using
D5% 0.45% saline or D5% 0.9% saline (in older children) should be administered.
Vital signs, urine output, and conscious level should be closely monitored. Hematocrit should
be monitored at least once a day or more often if required. Non-steroidal drugs or aspirin
should be avoided as it has been shown to aggravate platelet dysfunction and predispose to
severe and refractory bleeding.9 It is important to recognize that, in the majority, deterioration
occurs at the time of fever defervescence. In mild cases this might be accompanied
by mild changes in pulse rate and blood pressure, together with peripheral coolness and
congestion, suggesting a degree of hypovolemia secondary to plasma leakage (often with
mild elevations of hematocrit). This might recover spontaneously or after fluid therapy.
Hematocrit levels should return to normal accompanied by improvement in circulation once
appropriate fluids are given. There is no role for the prophylactic transfusion of blood
products such as platelets to correct thrombocytopenia. Preventive transfusions with
plasma
and platelets in an attempt to correct coagulopathy and thrombocytopenia does not
produce
sustained improvements in coagulation and platelet levels during the plasma leakage
phase of
DHF/DSS. Adequate management of shock prevented development of bleeding, even in those
who were not transfused.10 Reduce or discontinue intravenous fluids after 24–48 hours after
fever defervescence, due to the relatively short period of increased capillary permeability.
Continuing intravenous fluids at such rates is likely to lead to pulmonary edema or gross
edema. Convalescence is usually uncomplicated with gradual recovery of the platelet counts.

Management of dengue shock syndrome

In severe cases the patient’s condition suddenly deteriorates a few days after onset of fever,
with signs of circulatory collapse similar to our patient. Although this often happens between
day 3 and day 7 after onset of fever and whilst the fever is settling, 44% of children with DSS
have been found to be febrile (temperature 38–39 °C) at the time of shock.
One of the earliest sign is narrowing of the pulse pressure to ≤20 mmHg. Patients whose pulse
pressure is ≤10mmHg are those who are more likely to have prolonged shock and experience
subsequent episodes of shock after initial resuscitation. DSS is a medical emergency: prompt
and adequate fluid replacement is necessary to expand plasma volume. Rapid infusions of
20 ml kg−1 of crystalloids are given until circulation is restored. Positive pressure may be
required for rapid push of fluids. The infusion rate should be returned to normal once
hemodynamics are normalized and continuously adjusted based on frequent microhematocrit
assessments. The example in our patient would be as follows: Following initial bolus of 600 ml
0.9% saline (20ml kg−1), calculate intravenous fluids for mild tomoderate isotonic dehydration
(usually between 5 and 10%) based on 30 kg body weight.
Maintenance fluid ¼ ð10 _ 100Þ þ ð10 _ 50Þ þ ð10 _ 20Þ ¼ 1700 ml
5% deficit ¼ ð5 _ 30 kg _ 1000Þ=100 ¼ 1500 ml
Total fluids over 24 hours ¼ 1700 þ 1500 ¼ 3200
¼ 130 ml h_1 _ 1 of D5% 0:45% saline

Although the patient was deemed to be “stable” worrying signs remained, including a narrow
pulse pressure, tachycardia and an elevated hematocrit. Frequent assessment of hematocrit
would have detected a rise, which would have preceded the shock. In the event of a rise in
hematocrit with stable hemodynamics 300 ml of colloids could have been administered over
2–3 hours. It could have been possible that earlier administration of appropriate fluids would
have reversed or avoided development of irreversible shock with resulting bleeding and end-
organ failure.
From a state of compensated shock patients may pass rapidly into a profound state of
shock with imperceptible pulse and blood pressure, which may lead to a more complicated
course of tissue acidosis, gastrointestinal bleeding and end-organ failure. In these cases larger
volumes are required rapidly. An average of 134 ml kg−1 over 36–48 hours was required in
222 patients during a randomized trial of fluid resuscitation in DSS.12 This is in contrast to
the American College of Critical Care Medicine guidelines for resuscitation in pediatric and
neonatal septic shock which recommended the use of inotropes or pressors once >60 ml kg−1
of fluids is required.13 Inotropes are rarely required in DSS as the main pathophysiology of
shock is hypovolemia from massive capillary leak. The choice of fluids, however, remains
unclear. It would be reasonable to use 0.9% saline as initial resuscitation fluid and consider
colloids if volumes >40 ml kg−1 are required to correct shock. Ringer’s lactate, which was the
World Health Organization recommended fluid for resuscitation in DHF, performed the
least well in the aforementioned trial with the longest recovery time. A comparison of colloid
and crystalloid suggested benefits in children presenting with lower pulse pressures (i.e. those
in more severe states of shock) who received colloids.12

Management of intractable shock and transfusion of blood

In cases of persistent shock after adequate initial resuscitation with crystalloids andcolloids,
despite a decline in the hematocrit level, significant concealed internal bleeding (most often
gastrointestinal) should be suspected and fresh whole blood transfused. The amount
transfused should just be sufficient to raise the red blood cell concentration to normal.
Hemoconcentration often masks the degree of internal hemorrhage. The hematocrit (and
hemoglobin) would appear normal despite large GI bleeding. Vice versa, ongoing blood loss
and subsequent transfusion of whole blood would make assessment of plasma loss using
hematocrit difficult. In a patient with refractory shock/bleeding who has been transfused we
often choose a cut-off hematocrit (usually in the range of 0.4 to 0.45 depending on age), above
which we would transfuse colloids/crystalloids, below which we would transfuse red cells.
Transfusion of other blood products like cryoprecipitate, plasma, and platelets might be
needed at this time to correct the disseminated intravascular coagulopathy (DIC). Promising
treatment modalities in this subgroup include the use of recombinant activated factor VII.14
Factors that would make one suspect internal bleeding would be prolonged duration of shock
and low-normal hematocrit at diagnosis of shock. Additional factors would be the presence of
significant organ dysfunction at time of shock (suggesting prolonged shock) such as elevated
creatinine, hyperlactatemia, and DIC. Mechanical ventilation may be required due to increasing
respiratory distress from pleural effusion/ascites. Once the hematocrit has stabilized in the
region of 0.4, we would continue intravenous fluids, which should be reduced within 24 to 48
hours after onset of shock. Reabsorption of extravasated plasma occurs 2 to 3 days after, and
may cause hypervolemia, hypertension, and pulmonary edema in those still receiving fluids, or
in those who are in na oliguric phase of acute renal failure like our patient. This may require
diuretics or renal
replacement, respectively.

Additional points
1. Insertion of nasogastric tube and endotracheal tube carries the risk of trauma and
hemorrhage to nasal passages and stomach. If it is necessary, the oral route is preferable.
2. Insertion of intercostal drains carries the risk of trauma and hemorrhage to the lung. Careful
titration of intravenous fluids to achieve stable vital signs, with reduction of intravenous fluid
intake once stable vital signs are achieved, will limit the accumulation of large pleural
effusions, ascites, and positive fluid balance in children. Large pleural effusions during the
recovery phase after 48 hours may need small doses of frusemide.
3. Insertion of central venous line carries the risk of hemorrhage and should not be routinely
inserted.
4. The use of corticosteroids in the treatment of shock has failed to show any benefits.15
5. Echocardiogram assessment is recommended in cases of profound shock as a small
percentage have decreased function requiring inotropes and may also be useful to assess
volume status.

Learning points

1. A child from an endemic area with high fever, flushing without coryza and petechiae should
be suspected to have dengue infection.
2. Presence of thrombocytopenia and concurrent hemoconcentration is essential to the clinical
diagnosis of DHF/DSS.
3. The critical period is during fever defervescence, with a rising hematocrit (by ≥20 %)
indicating significant plasma loss and need for IV fluid therapy. Be wary that a percentage
might still be febrile during the critical period. Early and appropriate IV replacement can
prevent shock and modify severity.
4. Assessment of patient’s clinical state, together with micro-hematocrit assessment, can guide
treatment before the critical stage of shock occurs.
5. DSS is a state of hypovolemic shock secondary to large plasma losses. Replacement with
isotonic fluids like 0.9% saline and/or colloids is life-saving. Colloids may have advantages
over crystalloids.
6. Volume replacement should be guided by the rate of plasma leakage (clinical state,
hematocrit, urine output). There is no role of prophylactic transfusion of blood products.
7. Significant bleeding is often the result of prolonged shock, leading to tissue acidosis,
disseminated intravascular coagulopathy, and end-organ failure. Bleeding can be suspected in
patients with refractory shock and those with relatively low hematocrit at diagnosis of shock.
8. The duration of plasma leakage is for a period of 24–48 hours and over-replacement with
more volume and/or longer periods may lead to generalized edema and pulmonary
congestion, especially when reabsorption of extravasated plasma occurs.