Chapter Text
Avulsed both front teeth, age 7:
The maxillary alveolar region demonstrates acute avulsion of the deciduous central incisors, with teeth numbers 51 and 61 (the primary maxillary central incisors) completely displaced from their respective sockets. The gingival tissue immediately surrounding the resultant void exhibits pronounced inflammatory response, characterized by hyperemia, interstitial edema, and microtears along the free gingival margin. The alveolar sockets themselves are hemorrhagic, with the exposed trabecular bone partially lined by residual periodontal ligament fibers, torn from the cementum and lamina dura, leaving delicate, frayed strands adhering sporadically to the socket walls. Capillary networks within the spongiosa continue to extravasate blood, producing a mixture of bright red arterial and darker venous flow that pools within the sockets and partially seeps into the oral vestibule.
The interdental papillae have been disrupted, and the adjacent mucosa demonstrates reactive swelling. Microscopically, the periodontal ligament remnants reveal acute tearing, separation from the cemental surface, localized fibroblast injury, and exposure of Sharpey’s fibers. The alveolar bone, normally protected by soft tissue and ligamentous attachments, is transiently exposed, leaving the thin labial and palatal cortical plates susceptible to desiccation, microbial colonization, and early osteoclastic resorption.
Immediate neurovascular consequences are evident: branches of the superior alveolar nerves, which normally innervate the pulp and surrounding periodontium, are acutely deprived of their terminal sensory targets, generating sharp, radiating nociceptive signals along the maxillary arch and potentially producing transient paresthesia in the adjacent mucosa and upper lip. Small arteries and veins supplying the pulp chambers and periodontal ligament are disrupted, contributing to localized ischemia in residual tissues and amplifying the acute inflammatory response.
The oral environment further influences initial pathophysiology: salivary enzymes, combined with rapid bacterial colonization, initiate the early stages of wound healing, necessitating a swift transition from hemostasis to inflammation, granulation tissue formation, and eventual alveolar remodeling. Without timely intervention, the alveolar ridge may undergo dimensional loss, potentially complicating future orthodontic alignment or prosthetic replacement.
Functionally, the patient exhibits immediate impairment: absence of anterior occlusal contact, transient alteration in phonation, and exposure of the labial cortical plate, which is normally shielded by intact periodontal ligament and enamel. The surrounding soft tissues, though structurally preserved, are acutely sensitive to mechanical stress, temperature fluctuation, and chemical stimuli, reflecting combined activation of nociceptors and localized inflammatory mediator release.
At eight years old, Denny Whitaker sits cross-legged on his dorm room floor, holding the can of peaches in front of him like it’s a treasure chest. The label is half-peeled, the metal rim dented. He runs his finger over it, thinking. This has to last a week. One can. Seven days. He can do it, he’s absolutely sure.
See, nobody has forgotten him on purpose. Everyone at Yale assumes someone else is looking out for the eight-year-old genius. A dean thinks maybe the social worker is checking in. The social worker assumes the dorm supervisor is keeping tabs. The dorm supervisor assumes Denny’s professors are helping. But nobody is, so he drifts through the cracks, smiling with dimples, carrying his too-heavy backpack, invisible in plain sight. He likes it that way, it’s so much better than being noticed; being a target.
He flips open the Swiss army pocketknife he won at a math competition, it was in a hiking gift basket, and punctures the lid. The sweet smell escapes, and for a moment, he almost gives in to hunger, almost tips the can to his lips. But he doesn’t. He’s smarter than that.
He calculates: eight peach slices, syrup pooled at the bottom. He can ration one slice per day, saving the syrup for the in-between hours when his stomach claws at him. He finds an empty travel-sized shampoo bottle in the bathroom, rinses it, and pours in the syrup. Then he lines up the peach slices on a paper towel, patting them dry before tucking them back into the can, sealing it with a strip of duct tape.
Day one: he eats a single slice slowly, chewing until the sweetness fades. Day two: another, with half a capful of syrup. By day three, he’s dizzy with hunger during lecture, but he distracts himself by filling margins with equations, turning the ache in his stomach into numbers.
Each night, he tells himself the same thing: If I can make this last, I can make anything last.
He learns early on that nobody notices the quiet boy counting peach slices like currency. Nobody sees the real genius behind the dimples teaching himself how to exist, one rationed bite at a time. Nobody cares about him. He likes it that way.
Denny’s been bouncing from one foster home to another for as long as he can remember. He’s small for his age, with a halo of curly, mousy-brown hair that never seems to lie flat and dimples that betray him whenever he tries to look serious. But behind his gentle face is a mind so sharp it often frightens the adults around him. He thinks that’s why all his foster families hated him so much.
By seven, Denny discovers a secret: if you’re clever enough, you can turn intelligence into currency. He enters every spelling bee, math olympiad, debate tournament, and science fair within a fifty-mile radius. Each time he stands on a stage or sits, his legs dangling from a chair too big for him, he transforms. Equations unfold in his head like blooming flowers, arguments forming with crisp precision, and strange facts — memorized from hours of library books — spilling from him as if they’d been waiting forever to be spoken.
The prize money adds up. While other kids save up for game consoles or bikes, Denny quietly stacks scholarships like stepping stones. He carries a battered backpack that rattles with certificates and envelopes, each one proof that he can outwit the hand life has dealt him. Or the hands that continue to hurt him.
When Yale admits him at eight years old, the dean shakes his head in disbelief at the tiny boy with dimples, but signs the papers that grant him a full scholarship.
The state signs off too, declares him a ward, and moves on. So, Denny Whitaker, age eight, lives alone in a dorm room meant for a college freshman. He learns how to exist piece by piece. He teaches himself how to do laundry and learns how to budget by scribbling numbers on notebook paper, calculating how long a box of ramen can stretch. When he doesn’t understand how to cook something, he experiments until he gets it right — or feeds the mistake to the squirrels outside the library.
His professors adore him, although he doesn’t know why — he sits in the back row with his curls falling into his eyes, his feet dangling from chairs built for grown-ups. He never raises his hand first, but when he speaks, the room goes quiet. He’s both invisible and unforgettable. But nobody hurts him anymore; he takes care of himself by himself. He’s okay.
Only… the loneliness lingers.
On nights when the campus goes silent, Denny presses his forehead to his cold dorm room window and watches the glow of other students’ laughter in the quad below. He’s too young to join them, too smart to belong anywhere else. Yet he refuses to feel sorry for himself. Instead, he opens a book, sharpens his tiny nub pencil, and reminds himself: I can make something of this. I will.
Greenstick fracture of ulna and radius, age 4:
The patient’s left forearm presents a nuanced yet unmistakable skeletal compromise, characteristic of a greenstick fracture — a partial, incomplete disruption of cortical integrity. Unlike a complete transverse fracture, the bone’s structural continuity is partially maintained; one side of each shaft — specifically the radius and ulna along their diaphyseal regions — remains intact, while the opposite cortex exhibits an abrupt microfissure that propagates longitudinally, indicative of tensile stress exceeding the bone’s elastic limit but insufficient to produce full separation. Subperiosteal lifting is likely present at the site of maximal bending, producing a subtle yet palpable irregularity along the volar or dorsal surfaces of the forearm, which may be obscured by reactive swelling.
The overlying soft tissues respond immediately to this insult. A diffuse edema forms along the anterior and posterior compartments, the interstitial fluid engorged with serum, erythrocytes, and inflammatory mediators. The skin above the fracture assumes a taut, almost translucent quality, occasionally mottled with ecchymosis where capillaries rupture under tension or secondary trauma. Palpation would reveal localized tenderness, a firm, irregular ridge tracing the arc of the fracture, and a slight crepitus if gentle pressure mobilizes the partially fractured cortices against each other.
Vascular dynamics in the limb adjust subtly yet detectably. Microhemorrhages from the periosteal vessels infiltrate surrounding tissues, forming early subcutaneous hematomas, while reactive vasodilation produces warmth and erythema localized over the radius and ulna. Muscular compartments — brachioradialis, flexor carpi radialis, and extensor muscles — exhibit involuntary guarding, contraction patterns designed to limit torsion and further insult, but these same contractions exacerbate localized pain and may subtly deform the forearm’s visual alignment.
From a biomechanical perspective, the forearm’s longitudinal axis may reveal slight bowing toward the site of maximal cortical disruption, producing asymmetry that is visually imperceptible at first glance but measurable through careful inspection or radiographic imaging. Each movement of the wrist or elbow transmits microstrain to the partially fractured cortices, eliciting sharp nociceptive feedback along the periosteum and adjacent neurovascular bundles, most prominently the radial and ulnar sensory fibers. Even slight pronation or supination of the forearm mobilizes interstitial fluids along gravity-dependent paths, accentuating swelling and reddening of distal tissues.
At the microscopic level, osteocytes adjacent to the fracture experience mechanical deformation, triggering localized apoptosis and the recruitment of osteoblasts and osteoclasts for eventual remodeling. The periosteum, lifted subtly at the fracture apex, forms a provisional scaffold for callus formation, an early biological attempt to stabilize the partially compromised bone while preserving longitudinal integrity.
The interplay of incomplete cortical disruption, soft tissue reaction, and inflammatory signaling produces a forearm that is visually unremarkable to the untrained observer yet biomechanically precarious: a structure teetering between intact function and complete fracture, where every minor manipulation — lifting, twisting, or compressive force — exerts localized stress along an anatomically vulnerable trajectory, both palpable and physiologically consequential.
The library smells like paper and radiator heat and a layer of dust that’s been settling since before Denny was born. He loves it here — it’s the only place on campus where he can disappear completely, where the clicking keyboards and whispered page turns make a kind of camouflage. His sneakers dangle off the oversized oak chair, not touching the ground, and he hunches over a book that weighs almost as much as he does. His curls fall into his eyes as he scribbles tiny calculations in the margins of his notebook.
But he’s hungry. So hungry his hands tremble as he grips his pencil, the letters breaking into faint scratches instead of clear lines. He’s on day five of the peach plan. One slice per day, syrup in careful sips. He told himself he could handle it. He has, mostly — his brain is sharp enough to ignore the gnawing for a while. But now the world tilts.
He stands up to reshelve the book, because he’s the kind of kid who insists on putting things back in their proper place, and the ground tilts away from him. His knees lock, his body sways, and he grabs the shelf with one hand, hard enough that the metal rattles.
A grad student passing by — a tall girl with a messy bun and an armful of highlighted papers — pauses. She’s in her twenties, the sort of person who is perpetually overcaffeinated and under-rested, her eyes rimmed with fatigue but kind in a way Dennis doesn’t know what to do with. She watches him wobble, frowning slightly, and then she digs into her tote bag. “Hey, champ,” She comforts, crouching a little so she’s eye-level with him. Her voice is quiet but not condescending. She pulls out a red can of Coke, cold enough to bead condensation on her fingers. She presses it into his small hand. “Here. Sugar emergency.” She smiles.
Denny stares at it like she’s given him gold. His dimples pop, but he doesn’t smile fully. He doesn’t want to seem needy, doesn’t want to draw attention to the fact that nobody checks if he’s eating, sleeping, or surviving. He nods instead, polite, whispering, “Thank you,” in the most grown-up tone he can muster. He is a grown-up. He pops the tab with both hands, careful not to spill a drop, and the hiss of carbonation feels like a tiny miracle. He takes a sip, and the syrupy sweetness floods him, buzzing through his veins. His hands go steady. His vision clears. The room, for a moment, stops spinning.
The grad student doesn’t press him with questions. She doesn’t ask where his parents are, why he looks so pale, why his backpack has frayed straps and why he smells faintly of laundry detergent and library dust instead of home. She just gives him a small, tired smile, taps his book with her pencil, and says, “Keep going. You’re doing great, kid.”
Then she’s gone, weaving back into the stacks, papers balanced against her hip, leaving Dennis with the Coke and a strange, foreign warmth in his chest. He sits back down, pulls his notebook toward him, and writes again, the equations flowing steadier this time.
Nobody is supposed to notice him. He tries so hard not to bother anybody. But, at least he knows he’s doing it right.
Bloody nose and broken cheek, age 2:
The subject’s facial anatomy exhibits an acute and violent disruption, most prominently across the midface. The nasal structure — normally a delicate scaffold of cartilage and bone — is compromised at the bridge, where the osseocartilaginous junction bears a conspicuous fissure. From this point of insult, blood emerges not merely as a superficial stain but as a dynamic, almost physiologically articulate fluid. Initially, the hematic exudate forms a microfilm across the anterior nares, where capillaries, ruptured under mechanical stress, bleed both actively and via passive oozing. The viscosity of the blood fluctuates as it mingles with mucosal secretions, creating thin, sanguine strands that adhere to the philtrum before gravity overwhelms their adhesion, drawing them downward along the nasolabial folds. The smell of iron — ferrous ions volatilizing from freshly lysed erythrocytes — is pronounced, suggesting arterial contribution in addition to capillary effusion.
Adjacent to this, the malar prominence — specifically the zygomatic arch and its lateral extension — reveals a displaced fracture. Palpation would likely detect crepitus, a subcutaneous grating that signals discontinuity in cortical bone. The overlying soft tissue is swollen to an almost caricatured degree: interstitial edema has produced tensely stretched skin, demonstrating a spectrum of ecchymosis indicative of hemoglobin degradation over time. Deep violet, almost inky regions overlie the focal point of trauma, radiating outward into periorbital cyanosis and eventually tapering into verdant and ochre hues at the margins. Microabrasions and petechial hemorrhages pepper the surface epithelium, evidence of shearing forces at impact.
The physiological response compounds the visual spectacle. Inhalation through the compromised nares is labored, turbulent, and noisy, while exhalation propels blood droplets onto adjacent skin. The chemosis of the conjunctiva may become apparent if the trauma has induced periorbital vascular stasis. Thermal changes are subtle but measurable: hyperemia of the inflamed regions contrasts with relative pallor of unaffected surrounding skin, highlighting the localized inflammatory response. Microscopically, one could infer leukocyte infiltration in the dermal layers and microvascular thrombosis at the immediate site of contusion.
The combination of nasal hemorrhage and zygomatic disruption produces both acute nociception and long-term structural vulnerability. The nasolabial folds are distorted, the nasofrontal angle altered, and the cheek’s convexity replaced with asymmetry — a testament to the underlying skeletal compromise. The interplay of blood, serous fluid, and inflammatory exudate creates a reflective, glistening surface that accentuates the three-dimensional undulations of injury, while each involuntary movement — grimace, blink, or swallow — further mobilizes fluids along gravity-defined pathways, painting the face in a constantly shifting tableau of trauma.
The acceptance letter is just a sheet of paper, really — crisp white, heavy stock, black ink that curls into official serif letters. Denny sits cross-legged on the carpet of his dorm room, holding it like it might dissolve if he breathes too hard. Congratulations… admitted to Yale School of Medicine… He’s eleven, too young for half the things that have happened to him, too old to be thrilled like a child is supposed to be.
Nobody comes. Nobody claps him on the back, nobody says We’re proud of you, Denny. The dean signed the papers mechanically, as though they were a bureaucratic inevitability. The foster system barely blinked; he was, technically, still a ward of the state. His professors are busy grading, researching, publishing. His classmates — those brilliant twenty-somethings with already weary eyes — don’t know what to make of him. The child genius who always sits in the back, curls falling into his eyes, notebook brimming with meticulous notes, who slips out before the study groups begin.
So Denny celebrates by himself.
There’s a reception table downstairs, half-cleared away after a seminar. Platters of cut fruit drying at the edges, lukewarm coffee in silver carafes, and — on the very end of the white-draped table — a tray of cookies. Chocolate chip, big as his palm. He waits until no one is looking, then sidles over, curls shadowing his face. He slips his hand forward fast, like a magician’s trick, and scoops four cookies into the pocket of his hoodie. His heart hammers. Not from guilt exactly — more from the small thrill of taking something that isn’t technically meant for him, but that he feels he’s earned.
Back in his room, he lines them up on his desk: four golden-brown discs, chocolate smudges shining faintly in the lamplight. He calculates immediately — four cookies, seven days. He can cut each one in half, maybe in quarters, stretch the sweetness out. Celebration in increments.
That night, he pulls his laptop closer, balancing it on the edge of his knees, and clicks open YouTube. He types “Treasure Planet full movie” into the search bar, finds a grainy upload with Spanish subtitles, and lets it play. The screen’s glow spills over his curls, painting his face in shifting blues and golds as ships made of solar sails sweep across stars. He takes the tiniest bite of cookie. The sugar explodes on his tongue, overwhelming after weeks of starch and rationing. He chews slowly, eyes widening, as though his body has forgotten how to accept pleasure. After the second bite, his stomach twinges sharply — too much, too fast. He presses a hand to his belly, curls forward slightly, but keeps chewing anyway, because this is what he has. His celebration. His reward. He’s gonna eat them all.
The cookies hurt. His insides cramp with the sudden arrival of sweetness, a rebellion against starvation and his careful arithmetic. But Denny keeps watching Treasure Planet, jaw set, determined not to cry. The boy on the screen soars through galaxies, chasing freedom, finding belonging. Denny swallows the crumbs in his throat and imagines he’s there too, sailing among the stars, a kid with nobody behind him but still moving forward.
When the credits roll, the cookies are gone. Half of him aches — physically, in the hollow twist of his stomach — but half of him feels strangely, quietly triumphant. He has celebrated. Nobody noticed, nobody applauded, but he marked the moment.
Then, Denny Whitaker, eleven years old, newly admitted to Yale Medical School, sleeps alone in his dorm with nothing but the glow of his laptop screen as a nightlight.
Cut knee, rusty can, age 12:
The patient’s anterior knee demonstrates a laceration of variable depth, inflicted by a jagged metallic object, identified as a corroded can edge. The wound traverses the epidermis and dermis, producing a sharply defined incision with irregular margins. Surrounding skin exhibits reactive erythema and edema, consistent with acute inflammatory response. Microtears along the periwound tissue indicate shearing forces applied tangentially to the skin surface at the moment of contact.
Hemorrhage is both superficial and deeper, involving small dermal capillaries as well as subdermal venules, resulting in a mixture of bright arterial blood and darker venous blood within the wound bed. The exudate is partially diluted by interstitial fluid due to local edema, creating a moist wound environment. The exposed subcutaneous tissue demonstrates a disruption of connective tissue fibers, with visible adipocytes in the deeper layers where the cut has breached the dermal-subcutaneous junction. The wound margins may exhibit early fibrin deposition along the edge, an initial component of hemostasis.
Given the corroded nature of the implement, there is an increased risk of microbial inoculation. Rust particles adhering to the lacerated surfaces serve as potential fomites for Clostridium tetani and other opportunistic pathogens. Microscopically, bacterial colonization and early neutrophilic infiltration may occur within hours, producing localized inflammation, edema, and pain. The dermal nerve endings in the vicinity — primarily nociceptive free nerve endings — are acutely activated, generating sharp, radiating nociception throughout the anterior knee and possibly eliciting protective muscular contraction of the surrounding quadriceps and hamstring groups.
The knee joint capsule, patellar tendon, and underlying skeletal structures remain structurally intact, though deeper penetration could risk partial disruption of the prepatellar bursa, which would present with additional swelling, warmth, and restricted mobility. Immediate physiological response includes vasodilation, increased vascular permeability, and recruitment of inflammatory mediators such as histamine, prostaglandins, and cytokines, which collectively contribute to erythema, warmth, and edema.
Functionally, the patient experiences acute impairment in knee flexion and extension due to pain, localized swelling, and reflexive muscle guarding. Saline or exudate within the wound may facilitate the initial stages of clot formation while simultaneously increasing the risk of secondary contamination if left uncleaned. Without prompt wound care — irrigation, debridement, tetanus prophylaxis, and closure if indicated — there is a high likelihood of infection, delayed healing, and potential scarring or keloid formation.
His stomachache starts on a Monday morning, faint and sharp, a twist just below Denny’s ribs. He ignores it. He’s used to ignoring his body. His body is a noisy thing — always hungry, always tired, always smaller than it should be. What matters is the textbook in front of him, the stack of notecards he’s written out in his tiny, precise handwriting, the upcoming exam in pathology.
By Tuesday, the pain blooms bigger, like someone’s taken a fistful of barbed wire and knotted it inside his gut. He curls over his desk at night, cheek pressed to the wood, curls hanging into his eyes, but he keeps muttering terms under his breath. Rotavirus. Norovirus. Campylobacter. He almost laughs when he thinks about it — twelve years old, studying gastrointestinal disease while his own stomach is staging a rebellion.
Wednesday is worse. He hasn’t eaten since Monday except for half a granola bar and a bottle of water he stretched out like rations. The idea of food makes him gag, but the emptiness is worse. He goes to class anyway. His sneakers squeak faintly in the lecture hall, and he slips into his seat at the back. He takes notes with shaking hands, pausing every so often to curl into himself, invisible, silent. Nobody notices. They never do. He prefers it that way.
Thursday night, he curls on his dorm bed in the fetal position, dimples pressed into the pillow, whispering calculations. If it’s viral, it should peak in 72 hours. If it’s bacterial, maybe longer. If it’s foodborne, maybe self-limiting. He times his fever by counting the beats of his heart against his wristwatch. He keeps a record in a notebook: temperature, symptoms, water intake. His own tiny case study.
By Saturday, the pain is relentless, a saw blade inside him. He hasn’t slept properly in days. His hair clings damp to his forehead, and the hollow of his eyes is bruised with shadows. Finally, after six full days, he admits to himself he can’t just think his way out of it. He walks slowly, like an old man, to the campus health office.
The nurse is middle-aged, kind-faced but harried, papers stacked on her desk. She blinks when he walks in, small as he is, curls wild, face pale as paper. “Oh, honey,” She coos softly, “You don’t look so good. What’s going on?”
Denny tells her, clinical and clipped: “Epigastric pain for one week. Fever fluctuating between 100.8 and 102. Nausea. Poor oral intake.” His voice is steady, his dimples absent, his eyes downcast. He doesn’t say I’ve been alone this whole time.
She frowns, checks his forehead with the back of her hand, takes his temperature, listens briefly with her stethoscope. “Sounds like a bad tummy bug,” She says gently. She rummages in a drawer and presses two blister packs of Tylenol into his hand. “Take these. Stay hydrated. Follow up with your family doctor if it doesn’t improve.”
The words hang heavy. Family doctor, as though there’s someone he can call. Denny nods anyway, polite, dimples flickering when he forces a little smile. He doesn’t correct her. It’s easier not to.
He walks back to his dorm with the Tylenol rattling in his pocket like treasure. He swallows two with lukewarm tap water, lies down on his bed, and curls into himself. The pills won’t cure him, he knows, but they’ll blunt the edges. He stares at the ceiling until his eyes blur, whispering anatomy terms under his breath like lullabies.
Nobody checks in later. Nobody follows up. By Sunday, the fever breaks on its own, sweat soaking his pillow, body shivering as if expelling the sickness by sheer force. He drifts in and out of sleep, waking once to see the orange glow of sunrise creeping across the floor.
But the pain never really leaves.
By thirteen, Denny realizes it’s not a virus, it’s something else, something quieter but more insidious: an ache that comes and goes, sometimes a faint twist just under his ribs, sometimes a sharp spasm that folds him in half.
It becomes part of his routine, like sharpening pencils or making flashcards. He catalogs it, measures it, names it. “Dull ache, right upper quadrant, two hours postprandial.” “Acute cramp, epigastric, subsided with rest.” He records each episode in the margins of his notebooks. His med school notes are a strange hybrid — half textbook, half diary, the anatomy of the abdomen crisscrossed with his own data points.
Nobody asks about the shadows under his eyes, or the way he sometimes goes still in lecture, hand pressed flat against his stomach, curls falling forward to hide his face. His classmates assume he’s just tired, just overwhelmed. Professors see his test scores — always perfect — and never question.
At fourteen, during rotations, he learns to dissociate from the ache. He’s in Med Surg at three in the morning, shadowing residents who are barely awake, listening to the beep of machines. He watches a patient with appendicitis groan and curl up, and he feels a flicker of recognition. That’s me, too. Only no one’s watching.
He starts rationing food even more carefully. Not just because he’s always short on money, but because eating means risking the pain. He learns which foods flare it up — greasy things, dairy, sometimes even bread. He avoids them, scribbles a list in the back of his notebook, then scratches it out again when he realizes the rules keep changing.
By fifteen, it’s woven into his identity. His classmates joke about caffeine headaches, exam stress stomachaches. Denny smiles with dimples, nods along, but his is something different. His stomach is a weather vane: it flares before exams, during long nights, whenever he’s too happy, too nervous, too anything. It hurts like hunger but worse, as though it’s punishing him for needing anything at all.
Sometimes, late at night, he lies in bed with the laptop glow painting the curls around his face. He scrolls through PubMed articles far beyond his level, chasing diagnoses he doesn’t dare claim out loud. IBS. Ulcer. Gallbladder disease. Crohn’s. He reads until the words blur, until the ache is nothing but white noise, and then he falls asleep, face pressed into the textbook, alone.
The ache is his constant shadow. Denny has grown around it the way trees grow around fences, curling and compensating, never quite straight. It strikes him in the mornings sometimes, a dull pinch beneath his navel, enough to make him hunch over the sink as he brushes his teeth. Other days it waits until evening, flaring sharp after a meal he thought was safe. It ebbs, it flows, it rules him without killing him.
He decides he’s had enough of waiting.
Every night that semester, he sprawls across his dorm bed with two laptops open — the school-issued one balanced on his knees, and a secondhand one perched beside him, the screen cracked at the corner. PubMed on one, online anatomy atlases on the other. His notebooks multiply, pages dense with diagrams of the abdomen, cross-sections of blood supply, scribbled timelines of his own symptoms.
He charts his stomach like a battlefield. He notes onset, duration, pain scale, relief factors. He records bowel movements, appetite, fevers. He even times how long he can press a knuckle into McBurney’s point before the ache flares. He is meticulous, relentless, and tired. Always tired. At first, he blames the usual suspects: irritable bowel, ulcers, gallbladder disease. But nothing quite fits. The pain isn’t random enough for IBS, isn’t sharp enough for gallstones, isn’t constant enough for Crohn’s. He begins to circle back to something older, something simpler.
Appendicitis.
But not the catastrophic, call-an-ambulance kind they drill into first-year med students. Not the acute, textbook case with fever and rebound tenderness and a rush to the OR. This is subtler. Chronic appendicitis. Smoldering, intermittent, a slow flame that never quite burns out. Rare, debated, often dismissed. But as he flips through article after article, scrolling until his eyes ache, he recognizes himself in the words. He leans back against the wall, curls damp with sweat, stomach clutched in one hand, pencil in the other. This is it, he thinks. It has to be.
But what can he do? He imagines calling a doctor, sitting in a clinic, explaining himself. “I’ve had abdominal pain for three years. I think it’s chronic appendicitis.” He can already hear the polite skepticism. He can see the raised eyebrow, the quiet dismissal of a boy too small, too young, too alone.
He realizes something else then, as heavy as the ache itself: he has never actually had a primary care doctor. No pediatrician who watched him grow, no family physician who knew his history, no one who called to follow up. Foster homes didn’t come with checkups. Social workers had paperwork to file, not appointments to schedule. He has had shots at school, nurse visits when things got bad, the occasional urgent care trip if someone noticed he was Death’s doorstep sick. But a real PCP? Someone who knew his name and kept track of him? Never.
The realization sits cold in his chest.
He closes his laptops, stares at the cracked ceiling above his bed. Maybe someday, he thinks, the words quiet, fragile. Maybe someday when I have insurance. When I have a job. When I’m not just a name nobody remembers.
For now, he folds the notebook shut, places it neatly on the growing stack. Another case study. Another diagnosis made in silence and when the pain returns — because it always does — he presses his hand to his stomach, grits his teeth, and whispers, “Chronic appendicitis,” as though naming it is enough to hold it back.
Low blood sugar, age 10:
The patient presents with acute neuroglycopenic and adrenergic manifestations secondary to a precipitous decline in plasma glucose concentration. Following a prolonged post-absorptive period without caloric intake, circulating glucose levels fall below the homeostatic threshold required to sustain optimal cerebral function, typically <70 mg/dL (3.9 mmol/L), although symptomatic onset may vary according to individual metabolic reserve and prior glycemic excursions.
The central nervous system — entirely dependent on glucose as its primary substrate — rapidly senses the deficit. Neurons in the hypothalamic ventromedial nucleus detect the hypoglycemic state, triggering a sympathetic-adrenal response. Clinically, this manifests as diaphoresis, tachycardia, and cutaneous pallor, accompanied by tremulousness and fine motor dysfunction. The patient may report dizziness, lightheadedness, or a subjective sensation of “brain fog,” reflecting diminished synaptic activity and impaired neurotransmitter synthesis, particularly of glutamate and gamma-aminobutyric acid (GABA).
Peripheral adrenergic activation produces catecholamine release — epinephrine and norepinephrine — which further induces vasoconstriction in cutaneous vessels, glycogenolysis in hepatocytes, and lipolysis in adipocytes. Despite these compensatory mechanisms, insufficient substrate availability leads to progressive neuroglycopenia. The patient may experience cognitive slowing, difficulty concentrating, disorientation, and impaired judgment. Visual disturbances, such as blurred vision or tunnel vision, may occur due to transient retinal hypoglycemia.
Simultaneously, counterregulatory hormones — glucagon from pancreatic α-cells, cortisol from the adrenal cortex, and growth hormone from the anterior pituitary — attempt to restore euglycemia by stimulating hepatic gluconeogenesis and limiting peripheral glucose uptake. However, in the absence of exogenous carbohydrate intake, these mechanisms are delayed and often insufficient, prolonging neuroglycopenic symptoms.
Physiologically, repeated neuronal depolarization under hypoglycemic conditions results in increased excitatory signaling, while ATP-dependent ion pumps, deprived of glucose-derived energy, begin to fail. This contributes to autonomic dysregulation and, in severe cases, seizure activity or syncope. Mild tremors and palpitations are early harbingers of the metabolic stress imposed on both central and peripheral tissues, reflecting the body’s urgent attempt to maintain cerebral perfusion and energy homeostasis.
Clinically, the patient’s skin may feel clammy, with pallor accentuated by sympathetic-mediated vasoconstriction, while pulse rate rises as cardiac output attempts to compensate for reduced vascular glucose availability. Subjectively, intense hunger develops, accompanied by nausea or a sensation of weakness. Recovery is typically rapid upon ingestion of glucose, initiating an abrupt reversal of neuroglycopenia, sympathetic overdrive, and cognitive impairment.
The eight floor smells like mesothelioma and mildew. It’s a place like him; a place that everyone else has forgotten. Paint curls in long strips from the walls, exposing the dull bones of drywall underneath. The radiators don’t work; when winter settles into Pittsburgh, the air grows damp and cold, and his breath fogs when he exhales.
This is where Denny lives.
He found the empty wing by accident — he’d wandered a stairwell that creaked with disuse. At the top: a hallway half-blocked with old caution tape, the kind that flakes when you touch it. Beyond it: silence. Empty rooms with cracked linoleum floors, windows smudged opaque with grime, and the hollow hush of a place nobody’s walked in for years. It isn’t safe, not really. The tiles crunch under his sneakers. Some rooms still smell faintly of disinfectant, others of mouse droppings. But it’s his. Nobody checks. Nobody notices. Nobody tells the sixteen-year-old genius where he’s supposed to sleep now that he’s been moved from Yale to Pittsburgh for rotations. Dorms are for undergraduates, and the med school assumes housing must have been arranged somewhere else. Foster care assumes Yale is handling it. Yale assumes the state is. So, like always, Denny falls between the cracks.
He chooses one of the smaller patient rooms at the far end of the hall, a rectangle with a broken bedframe pushed into the corner. He drags the frame back to the center, spreads his thin blanket across the mattress, and pretends it’s normal. The blanket doesn’t quite reach the edges. At night, he curls tight, curls falling into his eyes, dimples pressing into his pillow as though even in sleep he’s trying not to take up space.
He keeps his belongings in his backpack — clothes folded into tight rolls, notebooks stacked neatly, pencils sharpened. His borrowed stethoscope lies across the top like a crown jewel. Every morning he pulls the backpack onto his shoulders and leaves looking like any other exhausted med student. Sometimes the pipes groan, startling him awake. Sometimes the ache in his stomach stirs him before dawn, forcing him to curl tighter around himself. On especially cold nights he puts on every layer he owns — three shirts, two pairs of socks, hoodie over hoodie — and tells himself he’s fine. He’s always fine.
From his window he can see the city in pieces: rooftops bruised with rust, smokestacks coughing into the sky, the faint shimmer of bridges lit at night. He props his chin on the sill and watches headlights crawl like fireflies along the streets below. He imagines the cars are ships on the Etherium, like in Treasure Planet, each one bound for a place he’ll never belong to.
Nobody knows he lives here. He doesn’t tell them. He doesn’t tell anyone, because if he does, someone might notice, and if someone notices, they might take even this away. Denny, sixteen years old, future doctor, prodigy, orphan, ward of nobody, living garbage, curls into an abandoned hospital bed in a wing seven floors above the PTMC emergency department and whispers to himself the same mantra he’s carried for years: I can make this last. I can make anything last.
Food poisoning, bad bologna, age 14:
The patient presents with acute gastrointestinal distress secondary to ingestion of lunch meat contaminated with pathogenic microorganisms, likely including Listeria monocytogenes, Salmonella spp., or Clostridium perfringens, facilitated by protein denaturation, bacterial proliferation, and toxin accumulation in expired meat products. The initial insult occurs in the upper gastrointestinal tract, where bacterial endotoxins and exotoxins interact with the mucosal epithelium, triggering a cascade of inflammatory and neuroimmune responses.
Upon ingestion, the contaminated meat introduces viable bacterial colonies and preformed enterotoxins into the stomach. Gastric acid provides limited sterilization, but the sheer bacterial load, coupled with acid-resistant strains, allows significant survival. The small intestine’s epithelial lining becomes the primary site of microbial adherence and toxin-mediated insult. Enterotoxins bind to enterocyte surfaces, perturbing tight junctions and increasing paracellular permeability, while simultaneously stimulating enterochromaffin cells to release serotonin (5-HT), which activates intrinsic enteric neurons and vagal afferents, precipitating nausea and vomiting.
The colonization of the intestinal lumen produces additional pathophysiological effects: bacterial replication and fermentation generate gas, leading to abdominal distension and cramping. Cytokines — particularly interleukin-1β, interleukin-6, and tumor necrosis factor-alpha — are released from activated mucosal immune cells, promoting localized inflammation and recruiting neutrophils to the lamina propria. This inflammatory milieu contributes to the characteristic diarrhea, which is frequently watery but may contain mucus or traces of blood, depending on the extent of epithelial damage.
The vascular and neuroendocrine systems respond rapidly. Fluid loss via vomiting and diarrhea produces intravascular volume depletion, triggering compensatory tachycardia, peripheral vasoconstriction, and activation of the renin-angiotensin-aldosterone system. Hypovolemia and electrolyte derangements — including sodium, potassium, and chloride depletion — compound cellular stress, affecting neuromuscular excitability and cardiac conduction. Fever, mediated by pyrogenic cytokines, reflects systemic immune activation and hypothalamic thermoregulatory set-point elevation.
At the cellular level, enterocytes experience disruption of membrane ion transporters due to toxin activity, particularly chloride channels and sodium-potassium ATPase pumps, leading to osmotic diarrhea. Bacterial adherence also disrupts microvilli, reducing absorptive surface area and further exacerbating malabsorption. In severe cases, systemic dissemination of bacteria or their toxins may occur, producing bacteremia, septicemia, or localized organ involvement such as mesenteric lymphadenitis or hepatosplenic inflammation.
Clinically, the patient exhibits nausea, projectile or retching vomiting, diffuse abdominal cramping, diarrhea, malaise, and diaphoresis. Neurological effects may include headache, lightheadedness, and transient hypotension due to acute fluid and electrolyte imbalance. The oral mucosa may appear dry and tacky, and skin turgor may be reduced, reflecting dehydration. Recovery is dependent on hydration, electrolyte replacement, and, in some cases, antimicrobial therapy. Untreated or severe cases risk progression to hypovolemic shock or systemic infection, particularly in immunocompromised or elderly patients.
The vending machine hums in the corner of the hospital cafeteria, its fluorescent light buzzing faintly, illuminating rows of food that might once have been fresh. Wrapped sandwiches sit sagging behind glass, their bread puckered at the edges, lettuce gone translucent. It’s nearly midnight, and Denny stands in front of it, clutching three wrinkled dollar bills in one hand. His hoodie hangs off his shoulders, baggy enough to swallow him, the navy Yale crest faded from too many washes. His pajama pants bunch around his ankles, and his sneakers are tied in double knots, frayed laces dragging. He looks more like someone’s kid dragged out of bed than a medical student.
He presses his forehead briefly against the cool glass, eyes on a turkey sandwich wrapped in waxy plastic. Three dollars, exact change. He can make it last two days if he eats half now, half tomorrow. It’s probably expired — everything in the vending machine usually is — but it’s food, and food is rare enough.
Behind him, a voice clears its throat. Low, gravelly, seasoned with fatigue.
“Kid.”
Denny stiffens, shoulders hunching. He turns slowly.
A man stands there, stocky build under a pair of black scrubs, gray curls wiry around his temples, freckles scattered across skin that looks weathered by decades of sun. His ID badge reads Jack Abbot, MD – Emergency Medicine. His arms are crossed over his chest, a posture that reads less threat and more authority born of habit.
“Those sandwiches,” Dr. Abbot says, voice stern but not cruel, “— are bad news. Nobody should eat those. You’ll regret it before you’re halfway through.”
Denny shrinks back instinctively, curls shadowing his face, fingers tightening around the money. He doesn’t answer. He never does when cornered. He just dips his chin, eyes flicking toward the floor, hoping the older man will get bored, will leave, will let him have the vending machine sandwich in peace. But Dr. Abbot doesn’t move. He squints at him, then jerks his head toward the hot food line, where the cafeteria workers are spooning out the last trays of mashed potatoes and chicken. “Come on. Real food’s still out. Don’t waste your money.”
Denny hesitates, heart rattling in his chest. He takes a few steps, almost against his will, following the doctor toward the line. The smell of hot food makes his stomach twist in both hunger and dread. He picks up a tray, fingers trembling, eyes darting nervously to the glowing price board. Entrées: $7.49. Sides: $2.49 each. Drinks: $1.79. His three crumpled dollars feel suddenly pathetic in his pocket. He edges backward, hoodie sagging around him, ready to retreat.
Dr. Abbot notices. He narrows his eyes. “What’s wrong?”
Denny shakes his head quickly. “N-Nothing.” His voice comes out thin, higher than he’d like. He hugs the tray to his chest, curls shielding his face.
Abbot studies him and to him, the picture is simple: a kid in pajamas, hoodie too big, nervous as a stray cat. Probably a patient’s family member — someone’s little brother waiting out the night upstairs. Not his problem, not really. But still.
“Here.” The attending reaches into his pocket, pulls out a battered leather wallet, and hands a twenty across the counter before Denny can protest. “Plate him up.”
The cafeteria worker, used to this kind of thing, loads the tray generously: chicken still steaming, a scoop of mashed potatoes, green beans that actually glisten. She slides it across to Denny, who stares at it like it’s unreal. His throat aches. He can’t remember the last time someone bought him hot food just because.
“Eat,” Dr. Abbot says simply, in that tone doctors use when they don’t want arguments. He pushes the tray closer.
Denny nods quickly, dimples flickering and then vanishing as he shrinks further into his hoodie. He mumbles, “Thank you,” barely audible, and scurries toward a corner table. He sits with his back to the wall, tray balanced on his knees, curls falling forward as though to hide the fact that he’s about to devour it all.
Across the room, Dr. Abbot watches for a moment, arms still crossed, expression unreadable. Just another kid keeping vigil, he thinks. Just another family member waiting out the night. He shakes his head and turns back toward the ED.
Denny eats slowly, carefully, the way he always does — rationing bites, memorizing the taste, bracing for the inevitable stomachache that will follow. But for now, the food is warm, the room is quiet, and for a few minutes, he feels less invisible.
It’s stupid, but he pretends his Dad bought it for him.
Mild hypothermia, from the heat going out again, age 9:
The patient exhibits early-stage hypothermia, defined by a core body temperature between approximately 35°C and 36°C (95–96.8°F). At this mild threshold, homeostatic thermoregulatory mechanisms remain largely intact, but subtle compensatory responses are engaged to preserve core temperature in the face of environmental heat loss.
Cutaneous vasoconstriction is evident, mediated by sympathetic adrenergic activation of alpha-1 receptors in the peripheral arterioles. This reduces blood flow to the extremities, thereby minimizing convective and conductive heat loss but producing perceptible peripheral pallor and coolness of the hands, feet, ears, and nose. Mild shivering — an involuntary, oscillatory contraction of skeletal muscle — may be present, generating thermogenic heat through increased ATP hydrolysis and elevated metabolic rate. These tremors are typically fine and intermittent at this stage.
Metabolically, basal oxygen consumption and energy expenditure are slightly elevated to support shivering thermogenesis. Mild hypoglycemia may occur if the individual has not eaten, due to increased glucose utilization in skeletal muscle to fuel shivering. Respiratory rate may increase subtly to support heightened metabolic demand, though oxygen saturation generally remains within normal limits.
Cardiovascular responses are early and modest: peripheral vasoconstriction elevates systemic vascular resistance, and heart rate may increase slightly due to sympathetic activation. Blood pressure is generally maintained, but subtle elevations in diastolic pressure can occur as arteriolar constriction redistributes blood toward central organs. Cerebral perfusion is preserved, and cognitive function remains largely intact, though mild difficulties in fine motor coordination or dexterity may be noticeable due to decreased temperature in peripheral nerves and muscles.
At the cellular level, enzymatic activity throughout the body is slightly slowed by reduced tissue temperature, but homeostatic mechanisms compensate, maintaining near-normal ATP production. Peripheral nerve conduction velocity may decrease modestly, contributing to the sensation of stiffness or clumsiness in the extremities. Sweat gland activity is minimally reduced as thermoregulatory feedback suppresses evaporative heat loss.
Behaviorally and subjectively, the patient may report early chills, a feeling of fatigue or lethargy, and transient mental cloudiness if exposure is prolonged. Skin may appear pale or slightly cyanotic at the tips of the fingers and toes. Without intervention — such as rewarming, insulating clothing, or caloric intake — continued heat loss could progress into moderate or severe hypothermia, wherein shivering becomes more pronounced, cardiac conduction slows, and cognitive impairment intensifies.