Grand Rounds KASABACH MERRIT SYNDROME

LITTLE RED
RIDING HOOD
A Case of Kasabach-Merrit Syndrome
Johanna Christine Lomuljo
1st Year Pediatrics Resident
1
Objectives
• 1. To present the treatment approach for a pediatric patient
presenting with a vascular lesion
• 2. To discuss the incidence, pathophysiology, clinical manifestations
and diagnosis of Kasabach Merrit Syndrome
• 3. To outline pharmacological and surgical treatment of Kasabach
Merrit syndrome
References:
• Bissonette, B, Luginbuel, I (2019)Syndromes: Rapid Recognition and
Perioperative Implications, 2nd edition
• Cheerva, C. (2020). Kasabach-Merrit Syndrome. Yaish, H(Ed). Medscape
• Fitzpatrick's Dermatology in General Medicine (2018) ; 8th edition
• Mahjan, P (2017). Kasabach-Merritt Phenomenon: Classic Presentation and

Management Options. Clinical Medicine Insights:Blood Disorders Volume 10: 1–5
• Adams, D; Frieden I (2019). Tufted angioma, kaposiform hemangioendothelioma,

and the Kasabach-Merritt phenomenon. Corona(ed), UptoDate
Outline of Presentation:
I. History and Physical Exam of Index Case
II. Salient Features of the Case
III. Approach to Diagnosis
V. Working diagnosis
VII. Discussion
i. Overview of Kasabach Merrit Syndrome
ii. Epidemiology
iii. Pathophysiology
iv. Clinical manifestations
v. Diagnosis
vi. Treatment and Prognosis
VIII. Course in the Ward for Index Patient
IX. Key Points
Once upon a time…
HISTORY
GENERAL DATA
NAME N.A
AGE 1d
SEX M
ADDRESS GOVERNOR GENEROSO
BIRTHDAY APRIL 26, 2021
NATIONALITY FILIPINO
RELIGION ROMAN CATHOLIC
INFORMANT MOTHER
RELIABILITY 90%
CHIEF COMPLAINT
RED-PURPLE LESION ON THE
ABDOMEN
HISTORY OF PRESENT OF ILLNESS
● Born term to a 28 year old G1P1 mother via

NSVD at local hospital
● Good cry and activity as claimed
● Patient was then noted to have purplish
discoloration over his abdomen hence was
referred for further evaluation and
management
PRENATAL HISTORY
● Prenatal check up started at 2 months AOG with an OB-Gyn

● Subsequent visits done at Local health center with a midwife
● Total of 9 visits
● Ultrasound done at 2 months and 7 months AOG with
unremarkable findings
● UTI at 2 mos AOG; given with Cotrimoxazole for 10 days
● Repeat urinalysis: Normal
● Prenatal Meds: Folic Acid, FeSO4, Calcium tab and
Multivitamins with good compliance
BIRTH/NEONATAL HISTORY
● Patient was born term to a G1P1 mother via NSVD at

Local Hospital
● During labor, there was noted increase in BP hence
was referred to another hospital and was given with
unrecalled medications
● Patient was born via NSVD with good cry and activity
as claimed
● Patient was noted to have red-purplish discoloration
over the abdomen hence was referred for further
evaluation and management
FAMILY HISTORY
(+) HPN – maternal side

(+) DM – Maternal Side
(-) Bronchial Asthma
(-) Cardiovascular Disease
(-) Cancer
(-) Hematologic disease
FEEDING HISTORY
● Breastfed
IMMUNIZATION HISTORY
● BCG
● HEP B
PAST MEDICAL HISTORY
● No Previous Hospitalization
● No Previous Surgery
PHYSICAL EXAM
Physical Examination
General (at the ER)
○ Awake, Not in respiratory distress
Temp 36.7C Length 45 cm

RR 39 cpm Weight 3.3 Kg
PR 148 bpm HC 35cm
O2 sat 98 % AC 33cm
Lubchencho Classification of the NB
Lubchencho Classification of the NB
BALLARD’S SCORE
BALLARD’S SCORE: 40 weeks
SKIN Pinkish, warm, good turgor
HEAD No caput, open flat fontanel, no overlapping of sutures,

no dysmorphism
EYES Anicteric Sclera, pinkish palpebral conjunctiva, PERRLA,

no discharge
EARS Symmetric with instant recoil, no discharges
NOSE No alar flaring, midline, patent
No cleft lip or palate,

MOUTH no ankyloglossia
CHEST
Equal chest expansion, clear breath sounds, no
/ retractions
Lungs
HEAR Adynamic precordium, Distinct heart sounds, no
murmur
T
Globular, non distended, palpable, red to

purple vascular lesion ~5x6cm over
Abdomen upper abdomen, warm, rubbery,
vascular, non pulsating, abdominal
girth 33 cm
Genitals Grossly male, descended testes
Extremitie No polydactyly, full pulses, CRT <2s

s
Salient Features
HISTORY PHYSICAL EXAMINATION
Newborn - red-purplish vascular lesion

Term over the upper abdomen,
Good cry and activity 5x6cm
Male
APPROACH TO DIAGNOSIS
Erythematous, non-scaling localized
lesions
Differential Rule in Rule out
Acne Can present at birth inflammatory papules or
Erythematous non-scaling pustules, usually on face
lesion and scalp.
-usually just 1-4 mm in
size
-does not present as firm
mass with the patient
Granuloma Annulare - characterized by skin- - Females more likely to
colored to violaceous be affected
lesions up to 5 cm in - Present as papules
diameter rather than firm mass
as the patient’s
- predilection for the
feet, ankles, lower
limbs, and wrists
- rope-like border and
central clearing
Erythematous, non-scaling localized
Differential Rule in lesions Rule out
Hemangiomas (based on
the patient’s age)
1. Congenital hemangioma - clinically present as fully - Cannot be ruled out at
developed lesions at the moment
birth
- present as bossed
plaques or masses (such
as in this patient) located
on the head, neck, or
limbs
2. Infantile hemangioma - may be present at birth - Usually seen in females
- most common tumor of - Cannot be ruled out at
infancy, occurring in 5% of the moment
newborns
-bright red, protuberant,
compressible, sharply
demarcated
lesions that may occur on any
area of the body
- lesions may be solitary or
multiple
Based on the appearance of the lesion and the known history of the
patient, hemangioma is a strong differential diagnosis.
However, it is notable that when diagnosing hemangioma, a myriad of

other similar looking lesions should also be taken into account.
Hemangiomas belong to a group called VASCULAR LESIONS, specifically

- VASCULAR TUMORS.
The Red Hood: CHILDHOOD VASCULAR
LESIONS
(International Society for the Study of Vascular Anomalies (ISSVA) Classification System )
Vascular
Vascular Tumors
Malformations
- Infantile Hemangioma
- Kaposiform - Capillary malformation
hemangioendothelioma - Venous malformation
- Tufted hemangioma - Lymphatic malformation
- Non-involuting congenital - Arteriovenous
- hemangioma (NICH) malformation (AVM)
- Rapidly-involuting - Mixed
congenital
- hemangioma (RICH)
“Little Red Riding Hood”: Vascular
Tumors
Differentials Rule in Rule out
1. Congenital hemangioma - clinically present as fully - Cannot be ruled out at the
developed lesions at birth moment
- present as bossed plaques or
masses (such as in this patient)
located on the head, neck, or limbs
2. Infantile hemangioma - may be present at birth - Usually seen in females
- most common tumor of - Cannot be ruled out at the
infancy, occurring in 5% of newborns moment
-bright red, protuberant,
compressible, sharply demarcated
lesions that may occur on any area of
the body
- lesions may be solitary or multiple
“Little Red Riding Hood”: Vascular
Tumors
Differential Rule in Rule out
3. Kaposiform - present at birth or develop in early Cannot be ruled out at the moment
hemangioendothelioma (KHE) childhood.
- appears as a slightly raised
subcutaneous mass with a purpuric,
bruised appearance and occasional
telangiectasias
4. Tufted angioma infiltrated, firm, dusky red to Lanugo hair hypertrichosis and increased
violaceous plaques or nodules with ill- sweating in the area overlaying the
defined borders. The size varies from tumor may be present (not seen in this
less than 1 cm to more than 10 cm. patient)
- typically located on the arms, legs, and
trunk Cannot be ruled out at the moment
5. Kasabach Merrit Syndrome - cutaneous blue, violaceous, or reddish- Cannot be ruled out at the moment
brown lesion
-usually presents at birth or in the
neonatal or early infancy period
- occurs in approximately 70 % of cases of
(KHE) and 10 % of tufted angioma
- Must be considered since this is a life-
threatening condition
“Little Red Riding Hood”: Vascular Tumors
Patient Infantile Kaposiform Tufted Congenital
hemangioma hemangioendothel hemangioma hemangioma
ioma
“What great big eyes you have”
Clinically, using our eyes, each of the vascular tumors could be considered for this
patient. This warrants further investigation.
DIAGNOSTICS
CBC
4/26/21 4/27/21 Normal values* (term
12th HOL neonates)
HGB 228 162 140-200
HCT 0.73 0.48 0.43-0.63
RBC 6.85 4.19 4.2-5.8
WBC 22.21 13.22 10.0- 30.0
Neutrophils 74 58 40-80
Lymphocytes 19 30 20-40
Monocytes 6 8 3-10
Eosinophils 0 4 1-8
Basophils 0 0 0-1
Platelet 53 40 150-350
MCV 97.8
MCH 32.7
*Source: Standards of Newborn Care, 4th Edition (2017)

D-DIMER Increased
Fibrinogen 2g/L
Ferritin 48.4ng/mL
CRP 4.970 (+) Less than
APTT 51.8 25.4-
59.8
PT 18 10-15.3
INR 1.37 0.53-
1.48
Blood Type O+
Whole abdomen ultrasound 4/26/21
(Outside)
Superficial soft tissue UTZ with Doppler
“THE BIG BAD WOLF”
What big teeth you have!
"The better to eat you with!"
The Big Bad Wolf:
• Aside from the vascular tumor, further testing revealed the following
diagnostic results were:
Thrombocytopenia Consumption
elevated prothrombin time
elevated D-dimer
Coagulopathy
The story so far…
Kasabach
Consumption
hemangioma Merrit
coagulopathy
Syndrome
“Little Red Riding “Big Bad Wolf”

Hood”
WORKING IMPRESSION:
• KASABACH MERITT SYNDROME;
• TERM BABY BOY DELIVERED VIA NSVD, APGAR SCORE 8,9, BALLARD
SCORE 39 WEEKS, APPROPRIATE FOR GESTATIONAL AGE
DISCUSSION
KASABACH MERRIT SYNDROME
• occasionally referred to as “hemangioma with thrombocytopenia” or “hemangioma thrombocytopenia
syndrome”, is a rare complication of hemangiomas in neonates and infants.
• Kaposiform-hemangioendothelioma and tufted angioma are the two forms of vascular neoplasms usually
associated with KMS.
Reference: Fitzpatrick's Dermatology in General Medicine (2018) ; 8th edition

KASABACH-MERRIT SYNDROME
Epidemiology:
Approximately 300 cases have been reported in the literature since
1940
• typically occurs in early infancy (< 1 year) or childhood,
• Almost all cases occur before 6 months of age.
• Boys and men are affected slightly more often than girls and women
• No racial predilection has been identified.
References:
Cheerva, C. (2020). Kasabach-Merrit Syndrome. Yaish, H(Ed). Medscape
Bissonette, B, Luginbuel, I (2019)Syndromes: Rapid Recognition and Perioperative Implications, 2nd edition
PATHOPHYSIOLOGY
• One hypothesis is that the abnormal endothelium and convoluted architecture of
the tumor vasculature promote platelet adhesion and trapping.
• The thrombocytopenia associated with vascular lesions is caused by a localized
consumption coagulopathy.
• The vascular lesion triggers an intravascular coagulation with platelet trapping,
consequent thrombocytopenia, and fibrinogen consumption and degradation, as
well as activation and consumption of coagulation factors, resulting in
disseminated intravascular coagulation (DIC). Activation of platelets also
promotes further growth of vascular tissue.
Reference: Cheerva, C. (2020). Kasabach-Merrit Syndrome. Yaish, H(Ed). Medscape

DIAGNOSIS
• The triad of thrombocytopenia, coagulopathy, and a vascular
tumor should be highly suggestive of KMS.
DIAGNOSIS
• Clinically, KMP is often marked by a rapidly enlarging tumor, which may be painful.
• laboratory evaluation is essential for the diagnosis.
• Complete blood count, fibrinogen, d-dimer, prothrombin time (PT), and activated partial thromboplastin time (aPTT).
• Kasabach-Merritt phenomenon is characterized by :

 very low platelet levels,
 fibrinogen levels decreased
 d-dimer and fibrin degradation products are elevated.
 PT & aPTT are typically normal to slightly elevated.
• Significant anemia can occur due to intralesional bleeding, coagulopathy, sequestration of blood within the
tumor, and/or hemolytic anemia secondary to the sheering of red blood cells in the abnormal vasculature of
the tumor.
DIAGNOSIS
• Biopsy
• Imaging Studies
• MRI – differentiate TA from KHE, main utility is to delineate the extent of disease and
document the response to treatment
CLINICAL MANIFESTATIONS
• Visible cutaneous blue, violaceous, or reddish-brown lesions are often
the presenting features in patients with Kasabach-Merritt syndrome
(KMS).
• Most lesions are located on the extremities.
• Some infants and older children with visceral lesions present with an
enlarged abdomen.
• These vascular lesions may continue to enlarge during the first 18
months of life.
CLINICAL MANIFESTATIONS
• The thrombocytopenia and consumption coagulopathy associated with
KMS may not initially be severe. However, symptoms may worsen as
the lesion enlarges and the infant grows. Affected infants may present
soon after birth or may not come to medical attention for several
months. The large volume of blood circulating through the lesion may
cause high-output congestive heart failure in infants.
• The natural history of KHE is that of slow regression, with the lesion
leaving a reddish-brown discoloration that often does not resolve
completely. It is unknown what percentage of KHE lesions develop
into KMS.
MANAGEMENT
Management:
• There are currently no consensus guidelines for the treatment of KMS. Some
studies have reported good therapeutic effects with comprehensive sequential
therapy, including steroid therapy, interferon, arterial embolization, vincristine,
radiotherapy, and surgery.
• There are no specific guidelines for diagnosis and treatment during the neonatal
period.
• At present, it has not been established which agent or combination of agents is
optimal. In many cases, multiple agents are given in sequence or in combination.
Reference: Adams, D; Frieden I (2019). Tufted angioma, kaposiform hemangioendothelioma, and the Kasabach-Merritt phenomenon. Corona(ed), UptoDate
Pharmacologic treatment
• Pharmacologic treatments include systemic steroids with or without vincristine as first-line therapy in most cases
• Vincristine is given at a weekly dose of 0.025 to 0.05 mg/kg for infants <10 kg and 1 to 1.5 mg/m for infants >10
kg for two months.
• Oral prednisolone 2 mg/kg or intravenous methylprednisolone 1.6 mg/kg is given daily.
• duration of therapy should be based upon each individual patient's response to treatment.
• goal is to taper off the corticosteroids to zero over four to eight weeks if there
• Vincristine is typically administered for 20 to 24 weeks
Reference: Mahjan, P (2017). Kasabach-Merritt Phenomenon: Classic Presentation and
Management Options. Clinical Medicine Insights:Blood Disorders Volume 10: 1–5
Surgical Management
• Surgical excision may be a second-line approach for tumors that have failed medical
management or for life-threatening tumors when the time to response to medical
therapy is considered too long.
• Embolization may be performed in conjunction with surgery to minimize bleeding
during resection.
• In life-threatening situations, embolization alone may provide a temporary reduction in
size of the tumor and allow more time for medical therapy to be effective.
Other management
• Hemostasis support: Platelets should not be given unless the patient is actively bleeding or in preparation for surgery
WHY? Because transfused platelets have a short circulatory time and may induce a rapid increase in size of the
tumor.
Several clinicians, including the authors, have observed rapid expansion of the lesion and increased pain following
platelet infusions, probably secondary to clotting in the small vessels of the tumor.
• Antifibrinolytic agents (tranexamic acid and aminocaproic acid) have been used in a few cases of KMS with mixed
results.
• Antiplatelet agents (aspirin, ticlopidine) are usually used in combination with other treatments such as systemic
corticosteroids and vincristine
• Propranolol has been suggested as a possible treatment for KMS, given its remarkable efficacy in the treatment of
infantile hemangiomas.
Reference: Adams, D; Frieden I (2019). Tufted angioma, kaposiform hemangioendothelioma, and the Kasabach-Merritt phenomenon. Corona(Ed), UptoDate
Is there a happy ending to this
story?
PROGNOSIS
• When KMS is promptly recognized and properly treated: the prognosis is usually
excellent because the DIC resolves as the vascular lesion recedes and because
KMS does not recur.
• When KMS goes untreated: mortality is 10-37%, primarily due to bleeding
secondary to the consumption coagulopathy.
• Besides bleeding, other conditions associated with morbidity and mortality are as
follows:
Visceral involvement (particularly in the retroperitoneal area and mediastinum)
Profound thrombocytopenia
DIC
Severe infection
Iatrogenic complications
To be continued…
EDUCATING THE FAMILY
• Given the various therapies available to manage KMP, a joint decision
by the physician and the family should be established regarding the
best approach.
• Side effects of the drugs administered should be discussed.
• Vincristine - peripheral neuropathy, constipation
• Steroids - hypertension, hyperglycemia, adrenal insufficiency, and
gastritis.
• Remind patient’s family that when KMS goes untreated: mortality is
10-37%, primarily due to bleeding
COURSE IN THE WARDS
In summary..
• Patient was admitted as a case of Kasabach Merrit Syndrome for a total of
19 days.
• Patient was given Propanolol, Prednisone and was supposed to be given
Vincristine, however parents did not consent.
• Patient was transfused multiple units of Fresh Frozen Plasma however
thrombocytopenia did not resolve.
• Patient was also given antibiotics and managed as a case of Neonatal Sepsis
since Blood GS/CS obtained revealed a growth of Staph. Hemolyticus
• Unfortunately, parents decided to bring patient home against medical
advice.
Monitoring of
Abdominal Lesion
size
Date Length Width
5/6 9.5cm 5.5cm
5/7 10cm 6 cm
5/8 9cm 6 cm
5/9 8 cm 6 cm
5/10 9 cm 5 cm
5/11 9 cm 5.5 cm
5/12 9 cm 6 cm
5/13 9 cm 5 cm
5/14 9 cm 5 cm
5/15 9 cm 5.5 cm
5/16 9 cm 5 cm
Fig 1. Patient’s lesion on Fig. 2 Patient’s lesion on day of
admission. discharge. 5/17 9 cm 5 cm
(4/27/21) (5/17/21)
Hospital Day 0 (4/27/21)
S O A P
Term red-purplish vascular Kasabach-Merritt Admit px to SN ward
Good cry and activity lesion over the upper Syndrome; Term Baby Boy For CBC, BT, Ferritin,
Male abdomen, 5x6cm Delivered Via Normal Fibrinogen, D-dimer, PT-
Noted red-purplish lesion Spontaneous Vaginal APTT, NPS/OPS, CXR
on abdomen Delivery, Apgar Score 8
&9, Ballard Score 39 Started on fluids
Weeks 3.2 Kilograms, TFI 80
Appropriate For D50W, D5IMB, CalGluc
Gestational Age
Referred to Hema Service
S O A P
Still with lesion on red-purplish vascular Kasabach-Merritt Hema Service
abdomen lesion over the upper Syndrome; Term Baby Boy Started on Prednisone
No other subjective abdomen, 5x6cm Delivered Via Normal 10mg/5ml, 1.7ml q12
complaints Spontaneous Vaginal
Delivery, Apgar Score 8 Start Ampicillin 50mkdose
&9, Ballard Score 39 Gentamicin 4mkdose
Weeks 3.2 Kilograms,
Appropriate For 15-L ECG
Gestational Age 2D echo
Blood GS/CS
S O A P
Stable VS red-purplish vascular Kasabach-Merritt Continue
(-)active bleeding lesion over the upper Syndrome; Term Baby Boy Prednisone 10mg/5ml,
(-) abdominal distenstion abdomen, 5x6cm Delivered Via Normal 1.7ml q12
Spontaneous Vaginal
Delivery, Apgar Score 8 Ampicillin- D1
&9, Ballard Score 39 Gentamicin D1
Appropriate For s/F 2D ECHO
Gestational Age
S O A P
No fever ECE, Kasabach-Merritt TFI 100
No bleeding red-purplish vascular Syndrome; Term Baby Boy Continue meds
No pallor lesion over the upper Delivered Via Normal CBC on D3 antibiotics
No losses abdomen, 5x6cm Spontaneous Vaginal Start continuous
Noted jaundice up to the Delivery, Apgar Score 8 phototherapy
chest &9, Ballard Score 39 Started on Propanolol
Weeks 3.2 Kilograms, 10mg tab+5ml. 1ml PO
Appropriate For now then q12 x 7 days
Gestational Age, Neonatal then increase to 2ml PO
Sepsis BIDx14 days
S O A P
Hemoglobin 199.0 ECE, Kasabach-Merritt Give Vit K 3.3mg 1:1
Hematocrit 0.57 red-purplish vascular Syndrome; Term Baby Boy dilution IVTT x 3 days
RBC Count H 6.22 lesion over the upper Delivered Via Normal
WBC Count H 12.33 abdomen, 5x6cm Spontaneous Vaginal Secure 3 units 50cc
Delivery, Apgar Score 8 aliquot off FFP
Differential Count &9, Ballard Score 39
Neutrophil 56 % Weeks 3.2 Kilograms, Repeat PT/PTT after Vit K
Lymphocytes 32 % Appropriate For
Monocytes 10 % Gestational Age, Neonatal Conferred plans with
Eosinophil 2 % Sepsis hema
Basophil 0 %
Platelet Count L 16
S O A P
s/p FFP transfusion ECE, Kasabach-Merritt Continue meds
(-) bleeding red-purplish vascular Syndrome; Term Baby Boy Discontinue phototherapy
(+) lightening of color of lesion over the upper Delivered Via Normal
vascular lesion, no abdomen, 5x6cm Spontaneous Vaginal
change in size Delivery, Apgar Score 8
&9, Ballard Score 39
Appropriate For
Gestational Age, Neonatal
Sepsis
S O A P
s/p FFP x 6 ECE, Kasabach-Merritt Syndrome; Continue meds
No bleeding red-purplish vascular lesion Term Baby Boy Delivered Via Discontinue phototherapy
Afebrile over the upper abdomen, Normal Spontaneous Vaginal Shift Ampicillin to
Latest CBC: 5x6cm Delivery, Apgar Score 8 &9, Ceftazidime
Ballard Score 39 Weeks 3.2 Shift Gentamicin to Amikacin
Hemoglobin 166.0 Kilograms, Appropriate For
Hematocrit 0.49 Gestational Age, Neonatal
RBC Count 5.30 Sepsis
WBC Count 9.44
Differential Count
Neutrophil L 38 %
Lymphocytes H 49 %
Monocytes 10 %
Eosinophil 3 %
Basophil 0 %
Platelet Count 13
MCH 31.3 pg
MCHC 33.6 g/dL
MCV H 93.2
S O A P
s/F FFP transfusion ECE, Kasabach-Merritt Syndrome; Continue present meds
red-purplish vascular lesion Term Baby Boy Delivered Via
over the upper abdomen, Normal Spontaneous Vaginal For Ultrasound of
5x6cm Delivery, Apgar Score 8 &9,
Ballard Score 39 Weeks 3.2
superficial soft tissue with
Kilograms, Appropriate For Doppler UTZ
Sepsis 2D echo done
S O A P
Good suck ECE, Kasabach-Merritt Syndrome; Continue meds
Good cry red-purplish vascular lesion Term Baby Boy Delivered Via To secure Vincristine from
Good activity over the upper abdomen, Normal Spontaneous Vaginal CCI pharmacy
(-) pallor Ballard Score 39 Weeks 3.2
S/F Soft tissue ultrasound
(-) bleeding episodes Kilograms, Appropriate For with Doppler studies
Sepsis Please measure size of
lesion on abdomen daily
once a day
S O A P
5.5x9cm Delivery, Apgar Score 8 &9,
Sepsis 2D echo done
S O A P
10x 6cm Delivery, Apgar Score 8 &9,
Sepsis 2D echo done
S O A P
Sepsis 2D echo done
S O A P
Good suck ECE, Kasabach-Merritt Syndrome; Continue present meds
Good cry red-purplish vascular lesion Term Baby Boy Delivered Via
Good activity over the upper abdomen, Normal Spontaneous Vaginal For Ultrasound of
9x5.5cm Delivery, Apgar Score 8 &9,
(-) pallor Ballard Score 39 Weeks 3.2
(-) bleeding episodes Kilograms, Appropriate For Doppler UTZ
Sepsis 2D echo done
S O A P
Good suck ECE, Kasabach-Merritt For Vincristine
Good cry red-purplish vascular Syndrome; Term Baby Boy Administration tomorrow
Good activity lesion over the upper Delivered Via Normal
(-) pallor abdomen, 9x5cm Spontaneous Vaginal
(-) bleeding episodes Delivery, Apgar Score 8
Appropriate For
Sepsis
S O A P
Good suck ECE, Kasabach-Merritt Continue present meds
Good cry red-purplish vascular Syndrome; Term Baby Boy
Good activity lesion over the upper Delivered Via Normal Undecided if Vincristine
(-) pallor abdomen, 9x5cm Spontaneous Vaginal will be given
Appropriate For
Sepsis
S O A P
Good activity lesion over the upper Delivered Via Normal Undecided if Vincristine
(-) pallor abdomen, 9x5cm Spontaneous Vaginal will be given
&9, Ballard Score 39 Contemplating HAMA
Appropriate For
Sepsis
S O A P
Good activity lesion over the upper Delivered Via Normal Did not consent to
(-) pallor abdomen, 9x5cm Spontaneous Vaginal Vincristine
&9, Ballard Score 39 Decided to go HAMA
Weeks 3.2 Kilograms, To complete antibiotics
Appropriate For then will send home
Sepsis
S O A P
Sepsis
S O A P
Sepsis
S O A P
Good suck ECE, Kasabach-Merritt Patient decided to go
Good cry red-purplish vascular Syndrome; Term Baby Boy home against medical
Good activity lesion over the upper Delivered Via Normal advice
(-) pallor abdomen, 9x5cm Spontaneous Vaginal
Appropriate For
Sepsis
• The end

Grand Rounds KASABACH MERRIT SYNDROME

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LITTLE RED

• Mahjan, P (2017). Kasabach-Merritt Phenomenon: Classic Presentation and

• Adams, D; Frieden I (2019). Tufted angioma, kaposiform hemangioendothelioma,

● Born term to a 28 year old G1P1 mother via

● Prenatal check up started at 2 months AOG with an OB-Gyn

● Patient was born term to a G1P1 mother via NSVD at

(+) HPN – maternal side

Temp 36.7C Length 45 cm

SKIN Pinkish, warm, good turgor

HEAD No caput, open flat fontanel, no overlapping of sutures,

EYES Anicteric Sclera, pinkish palpebral conjunctiva, PERRLA,

EARS Symmetric with instant recoil, no discharges

NOSE No alar flaring, midline, patent

No cleft lip or palate,

Globular, non distended, palpable, red to

Genitals Grossly male, descended testes

Extremitie No polydactyly, full pulses, CRT <2s

Newborn - red-purplish vascular lesion

However, it is notable that when diagnosing hemangioma, a myriad of

Hemangiomas belong to a group called VASCULAR LESIONS, specifically

HGB 228 162 140-200

HCT 0.73 0.48 0.43-0.63

RBC 6.85 4.19 4.2-5.8

WBC 22.21 13.22 10.0- 30.0

*Source: Standards of Newborn Care, 4th Edition (2017)

“Little Red Riding “Big Bad Wolf”

Reference: Fitzpatrick's Dermatology in General Medicine (2018) ; 8th edition

Reference: Cheerva, C. (2020). Kasabach-Merrit Syndrome. Yaish, H(Ed). Medscape

• Kasabach-Merritt phenomenon is characterized by :

5/6 9.5cm 5.5cm

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