2d:I[856015,["/_next/static/immutable/chunks/1xzisbplk9czp.js","/_next/static/immutable/chunks/3j2i1faptc_-9.js","/_next/static/immutable/chunks/0fma7nlq6immz.js","/_next/static/immutable/chunks/08tq8rmv423j5.js","/_next/static/immutable/chunks/1chr5wkk3j58k.js","/_next/static/immutable/chunks/37kmmh_zm4dov.js","/_next/static/immutable/chunks/311zvdjfxff-f.js","/_next/static/immutable/chunks/1a_hqhrsle_n_.js"],"default"] 2e:T5434,

Summary Table

Feature	Caput Succedaneum	Cephalhematoma	Subgaleal Hematoma
Risk Factors	Prolonged labor, vacuum-assisted delivery	Forceps or vacuum-assisted delivery, prolonged second stage	Vacuum extraction (strongest association), difficult instrumental delivery, coagulopathy
Etiology	Subcutaneous edema/serosanguinous fluid above the periosteum, external to the aponeurosis	Subperiosteal hemorrhage (between periosteum and skull bone)	Bleeding into the potential space between the periosteal aponeurosis (galea) and the periosteum
Patient Presentation	Soft, diffuse scalp swelling present at birth	Firm, well-circumscribed swelling appearing hours after birth	Progressive, fluctuant swelling that increases after birth; may present with signs of hypovolemic shock
Classic Physical Exam	Boggy, pitting edema that crosses suture lines; may cross the midline; poorly defined borders	Firm, tense collection that does not cross suture lines; well-defined borders limited to one cranial bone	Fluctuant swelling that crosses suture lines; ballotable fluid wave; swelling increases over hours; may see periauricular or periorbital ecchymosis
Key Diagnostic Results	Clinical diagnosis; no imaging required	Clinical diagnosis; skull X-ray may show linear skull fracture (5-25% of cases)	Clinical diagnosis supported by serial head circumference measurements; CBC, coagulation studies; CT if concern for intracranial extension
Management	Observation only; resolves spontaneously in days	Observation; no aspiration; monitor for jaundice	Emergency: fluid resuscitation, blood transfusion, correction of coagulopathy; pressure bandage to the scalp
Keywords	"Diffuse swelling at birth," "crosses suture lines," "pitting edema," "resolves in days"	"Does not cross suture lines," "appears hours after birth," "calcified rim weeks later"	"Vacuum extraction," "increasing head circumference," "ballotable fluid," "hemodynamic instability in a newborn"

1. Pathophysiology

All three lesions arise from trauma to different anatomical layers of the neonatal scalp. To understand them, you must know the five layers of the scalp, classically remembered by the mnemonic SCALP: Skin, dense Connective tissue, Aponeurosis (galea aponeurotica), Loose areolar connective tissue, and Periosteum. Each of these lesions occupies a different layer, and the layer involved dictates the clinical behavior.

Caput succedaneum is hemorrhagic edema in the subcutaneous tissue, which sits superficial to the aponeurosis. Because this layer is above the periosteum and not bound by any bony attachment, the fluid collection freely crosses suture lines and even the midline. It results from prolonged pressure of the presenting part against the dilating cervix, which obstructs venous return and causes extravasation of serosanguinous fluid. The swelling is present at birth because it develops during labor. It is benign and self-limited because the fluid is small in volume and reabsorbs within 2 to 3 days.

Cephalhematoma is a subperiosteal hemorrhage, meaning the blood collects between the periosteum and the outer table of the skull. Because the periosteum is tightly adherent to the skull at the suture lines, the hemorrhage is confined to a single cranial bone and cannot cross sutures. This is the single most important distinguishing feature on an exam. The bleeding is venous in origin, arising from rupture of small emissary veins during delivery. Because the accumulation is gradual, the swelling typically becomes apparent hours to a day after birth, not immediately. Over weeks, the periphery of the hematoma may calcify, creating a palpable calcified rim that can be mistaken for a depressed skull fracture. Important to note: an underlying linear skull fracture is present in roughly 5 to 25% of cases.

Subgaleal hematoma is the most dangerous of the three. The bleeding occurs in the loose areolar tissue between the galea aponeurotica and the periosteum. This potential space is enormous, extending from the orbital ridges anteriorly to the nuchal ridge posteriorly and laterally to the temporal fascia. Because of its vast capacity, it can accommodate a volume exceeding the total blood volume of a neonate ($\approx 80\text{ mL/kg}$). A full-term 3.5 kg newborn has approximately 280 mL of total blood; a subgaleal hematoma can sequester well over this amount, leading to hemorrhagic shock and death if not recognized early. The mechanism is shearing of emissary veins that bridge the subgaleal space, most commonly caused by vacuum-assisted delivery. Coagulopathy (including hemophilia and vitamin K deficiency bleeding) greatly amplifies the risk.

2. Classification and Clinical Manifestation

Feature	Caput Succedaneum	Cephalhematoma	Subgaleal Hematoma
Anatomical Layer	Subcutaneous tissue (above aponeurosis)	Subperiosteal (between periosteum and bone)	Sub-aponeurotic (between galea and periosteum)
Onset	Present at birth	Hours after birth	Hours after birth, progressively worsening
Crosses Suture Lines?	Yes	No	Yes
Consistency	Soft, pitting, boggy	Firm, tense, non-pitting	Fluctuant, ballotable fluid wave
Borders	Poorly defined, diffuse	Well-circumscribed, limited to one bone	Poorly defined, may extend to dependent areas
Skin Appearance	May show bruising, molding	Skin color usually normal	Ecchymosis may track to periauricular or periorbital regions
Change Over Time	Decreases from birth	Stable or slowly increases over first day, then resolves over weeks	Progressively increases; head circumference rises
Volume of Blood Loss	Negligible (mostly edema)	Limited (periosteal boundary); rarely causes anemia	Potentially life-threatening (>260 mL possible)
Associated Complications	None significant	Jaundice from resorption of hematoma; rare anemia; underlying skull fracture	Hypovolemic shock, DIC, death
Resolution	2 to 3 days	2 weeks to 3 months (may calcify)	Days to weeks if survived; requires active management

The clinical differentiation on exam vignettes almost always hinges on three variables: (1) does it cross suture lines, (2) when did it appear relative to birth, and (3) is the infant hemodynamically stable or deteriorating.

3. Diagnostic Workup

Test	Caput Succedaneum	Cephalhematoma	Subgaleal Hematoma
Best Initial Test	Clinical exam (no testing needed)	Clinical exam	Clinical exam + serial head circumference
Labs	None	Bilirubin if jaundice develops	CBC, coagulation panel (PT, aPTT, fibrinogen), type and crossmatch
Imaging	None	Skull X-ray if fracture suspected	CT head if intracranial hemorrhage suspected
Confirmatory Test	Not applicable	Ultrasound (if needed to differentiate from subgaleal)	CT scan or MRI

Caput succedaneum is a purely clinical diagnosis. The vignette will describe a soft, diffuse swelling present at birth that crosses suture lines. No workup is needed. If you see a question ordering imaging or labs for caput, the answer is observation.

Cephalhematoma is also primarily clinical. The key scenario where workup becomes relevant is when the question asks about complications. If the hematoma is large or the infant develops jaundice on day 2 to 3, you should check serum bilirubin because the resorption of blood products generates an unconjugated bilirubin load. A skull X-ray is indicated when there is clinical concern for an underlying fracture (roughly 5 to 25% association), particularly if the mechanism involved forceps delivery or significant trauma. Some sources recommend cranial ultrasound to differentiate a cephalhematoma from a subgaleal hematoma when the clinical exam is ambiguous.

Subgaleal hematoma is the one that demands urgent workup. The best initial step is serial measurement of head circumference, because an increase of more than 1 cm per measurement interval strongly suggests ongoing bleeding. Laboratory studies should include a complete blood count (to quantify blood loss), a coagulation panel (PT, aPTT, fibrinogen, and platelet count) to rule out underlying coagulopathy or evolving DIC, and a type and crossmatch in anticipation of transfusion. A CT scan of the head is indicated if there is concern for intracranial extension of the hemorrhage or an associated skull fracture.

A high-yield test-writer move: a vignette that describes a vacuum-delivered infant with progressively increasing head circumference, pallor, and tachycardia is testing whether you recognize subgaleal hematoma as a surgical/resuscitative emergency rather than dismissing it as a benign cephalhematoma.

4. Management and Treatment

Condition	Acute Management	Long-Term / Supportive
Caput Succedaneum	Observation only	Reassurance to parents; resolves in 2 to 3 days
Cephalhematoma	Observation; never aspirate (risk of infection/abscess)	Monitor bilirubin; phototherapy if jaundice develops; observe for calcification
Subgaleal Hematoma	ABC stabilization, IV fluid resuscitation (normal saline 10 to 20 mL/kg bolus), packed RBC transfusion, FFP and platelets if coagulopathy/DIC present	NICU admission, serial head circumference, serial hemoglobin, neurosurgical consultation if intracranial extension suspected

Caput succedaneum requires no intervention. The next best step in management on any exam question is reassurance and observation. There is no role for aspiration, compression, or imaging.

Cephalhematoma also requires observation, but the management section has two critical pearls. First, never aspirate a cephalhematoma. Aspiration introduces infection risk and converts a sterile, self-resolving hematoma into a potential abscess or osteomyelitis. This is a commonly tested trap. Second, because the large volume of sequestered blood undergoes hemolysis and generates unconjugated bilirubin, infants with large cephalhematomas are at increased risk for neonatal jaundice requiring phototherapy. The hematoma itself resolves over 2 weeks to 3 months. Peripheral calcification is common and benign; it remodels over months and does not require surgery.

Subgaleal hematoma is a true neonatal emergency. The next best step is hemodynamic resuscitation. Volume replacement begins with normal saline boluses (10 to 20 mL/kg, repeated as needed), followed by packed red blood cell transfusion (10 to 15 mL/kg) when hemorrhagic shock is evident (tachycardia, pallor, poor perfusion, falling hemoglobin). If coagulopathy is present (prolonged PT/aPTT, low fibrinogen, thrombocytopenia), administer fresh frozen plasma (10 to 15 mL/kg) and platelet transfusion as indicated. Vitamin K (1 mg intramuscular) should be confirmed or administered if there is any doubt about prior prophylaxis. A compressive head bandage (elastic wrap) can be applied to tamponade the subgaleal space and slow ongoing bleeding. The infant must be admitted to the NICU with continuous monitoring and serial hemoglobin checks every 4 to 6 hours.

5. Differential Diagnosis and Distractors

Differential	Why It Is Confusing	Key Discriminator
Caput vs. Cephalhematoma	Both are scalp swellings in newborns after delivery	Caput crosses suture lines, is present at birth, soft/pitting; cephalhematoma does not cross sutures, appears hours later, firm/non-pitting
Cephalhematoma vs. Subgaleal Hematoma	Both appear after birth and may follow instrumental delivery	Cephalhematoma is stable, limited to one bone, infant is well; subgaleal hematoma is progressive, crosses sutures, and the infant shows signs of shock
Subgaleal Hematoma vs. Caput Succedaneum	Both cross suture lines	Caput is present at birth and decreasing in size; subgaleal hematoma appears after birth and is increasing, with hemodynamic compromise
Cephalhematoma vs. Depressed Skull Fracture	A calcified cephalhematoma rim can feel like a bony step-off	Skull X-ray or CT distinguishes them; a calcified rim has a raised outer edge with a soft center, while a depressed fracture shows inward displacement of bone
Cephalhematoma vs. Meningocele/Encephalocele	Both present as scalp masses in neonates	Meningocele/encephalocele is midline, transilluminates, and has a pulsatile quality with increased intracranial pressure; cephalhematoma is lateral over the parietal bone

6. Traps and High-Yield Pearls

The single most tested concept in this topic is anatomical layer recognition. The exam writer wants to know whether you can correctly assign a scalp lesion to its layer based on two or three clinical clues: does it cross suture lines, when did it appear, and is the infant stable? Students most commonly get questions wrong by confusing cephalhematoma with subgaleal hematoma. Both can follow vacuum delivery, both appear after birth, and both involve blood. The key differentiator is trajectory: cephalhematoma is stable and benign, while subgaleal hematoma is progressive and potentially fatal.

Another common trap: a question asks for the next step in managing a cephalhematoma, and the distractor answer is "needle aspiration to relieve pressure." This is always wrong. Never aspirate a cephalhematoma.

Watch for the vignette that buries the critical clue: "a newborn delivered by vacuum extraction is noted to have a progressively enlarging scalp swelling with pallor and tachycardia." Students who latch onto "scalp swelling after vacuum" may jump to cephalhematoma and select observation. The words progressively enlarging and pallor/tachycardia are the test writer's signal that this is a subgaleal hematoma, and the answer is emergent resuscitation, not observation.

Finally, remember that cephalhematoma is a risk factor for hyperbilirubinemia. If the vignette describes jaundice developing on day 2 to 3 in an infant with a known cephalhematoma, the next step is checking total serum bilirubin and initiating phototherapy if indicated. The bilirubin load from hemolysis of the hematoma is the tested mechanism.

1e:["$","$L2d",null,{"article":{"id":"65a19992-cf89-4548-bfae-ff7b5b8b9644","title":"Trauma Kepala Neonatus","content":"$2e","category":"Reproduksi","created_at":"2026-05-16T07:51:03.292561+00:00","status":"published","subcategory":null},"questionCount":1,"sections":[{"id":"section-pathophysiology","num":"01","title":"Pathophysiology"},{"id":"section-classification-and-clinical-manifestation","num":"02","title":"Classification and Clinical Manifestation"},{"id":"section-diagnostic-workup","num":"03","title":"Diagnostic Workup"},{"id":"section-management-and-treatment","num":"04","title":"Management and Treatment"},{"id":"section-differential-diagnosis-and-distractors","num":"05","title":"Differential Diagnosis and Distractors"},{"id":"section-traps-and-high-yield-pearls","num":"06","title":"Traps and High-Yield Pearls"}],"hasSummaryTable":true}]