Cushing Syndrome

Populations and Risk Factors

Iatrogenic (exogenous) Cushing syndrome is overwhelmingly the most common form — any patient on long-term systemic corticosteroids (prednisone, dexamethasone, hydrocortisone) for more than 2–3 months is at risk; prevalence mirrors the large population of patients treated with chronic steroids for asthma, COPD, lupus, RA, inflammatory bowel disease, and organ transplant rejection
Endogenous Cushing syndrome is rare (2–3 per million per year); Cushing disease (pituitary ACTH adenoma) accounts for 70% of endogenous cases; affects women 3–8 times more than men; peak incidence ages 20–50
Adrenal tumors (adenoma or carcinoma) account for 15–20% of endogenous cases
Ectopic ACTH secretion (small cell lung carcinoma, carcinoid tumors) accounts for 10–15% — more common in men; often presents acutely with severe hypokalemia and metabolic alkalosis
Approximately 20% of Cushing syndrome patients have developed diabetes mellitus by the time of diagnosis — cortisol's gluconeogenic effects directly oppose insulin
Depression and cognitive dysfunction are common comorbidities (50–80%) from cortisol's direct CNS effects

Causes and Pathophysiology

Normal Cortisol Physiology

Cortisol is the body's primary glucocorticoid, produced by the adrenal cortex under ACTH regulation from the anterior pituitary (which itself is regulated by CRH from the hypothalamus). Cortisol has wide-ranging effects on metabolism, immune function, fluid balance, and connective tissue.
Normal cortisol functions include: stimulating gluconeogenesis (raising blood glucose), promoting protein catabolism (liberating amino acids for gluconeogenesis), facilitating fat redistribution, suppressing inflammatory and immune responses, and maintaining vascular reactivity to catecholamines.
Cortisol follows a diurnal rhythm — highest in the early morning, lowest at midnight. Chronic stress, medications, and tumors can override this rhythm.

Exogenous (Iatrogenic) Cushing Syndrome

Long-term administration of exogenous glucocorticoids (prednisone, prednisolone, dexamethasone, methylprednisolone) at supraphysiological doses suppresses the HPA axis through negative feedback. The adrenal glands atrophy from disuse.
The cushingoid features develop progressively — typically noticeable after 2–3 months of continuous systemic steroid use at doses exceeding the physiological equivalent of 7.5 mg prednisone daily.
Critical safety point: abrupt discontinuation of long-term steroids can precipitate adrenal crisis (acute adrenal insufficiency) because the atrophied adrenals cannot resume cortisol production quickly enough. Steroid tapering must be medically supervised. Massage therapists should never advise stopping or reducing corticosteroid medications.

Why Proximal Muscle Wasting Develops

Cortisol promotes protein catabolism by activating ubiquitin-proteasome pathway enzymes that break down muscle proteins. The catabolized amino acids are redirected to hepatic gluconeogenesis.
Type II (fast-twitch) muscle fibers are preferentially affected (higher protein turnover rate) — and proximal muscles (pelvic girdle, thigh, shoulder girdle, upper arm) contain a higher proportion of Type II fibers than distal muscles.
The result is the characteristic "spindly extremities" — proximal limb muscles visibly waste while central fat accumulates, creating the apple-shaped body habitus. Functional limitations include difficulty climbing stairs, rising from chairs, and lifting overhead.
Clinical distinction from other myopathies: Cushing myopathy is painless (unlike inflammatory myositis which is painful and tender, and unlike hypothyroid myopathy which is stiff and achy). CK is typically normal (protein is being catabolized, not leaking from damaged membranes).

Why Central Fat Redistribution Occurs

Cortisol has complex, region-specific effects on adipose tissue. In visceral and cervicofacial fat depots, cortisol stimulates both adipogenesis (new fat cell formation) and lipogenesis (fat storage). In peripheral subcutaneous fat (limbs), cortisol promotes lipolysis (fat breakdown).
This produces the characteristic redistribution: fat accumulates centrally (abdomen, face, supraclavicular fossa, cervicodorsal region) while peripheral fat is lost. The buffalo hump is a cervicodorsal fat pad that develops over the C7–T2 spinous processes.
Postural consequences: the buffalo hump shifts the cervicothoracic weight balance anteriorly, driving forward head posture and increasing thoracic kyphosis. Central obesity shifts the center of gravity forward, increasing lumbar lordosis compensatorily. This entire postural chain — forward head, increased kyphosis, increased lordosis, pendulous abdomen — is characteristic and affects positioning, bolstering, and treatment approach.

Why Skin Becomes Fragile

Cortisol directly inhibits fibroblast collagen synthesis while simultaneously increasing collagenase activity (collagen breakdown). The net result is progressive thinning of the dermal collagen matrix — skin becomes paper-thin, translucent, and tears under forces that would be harmless to normal skin.
The same mechanism produces purple striae (stretch marks) — the thinned dermis splits under the mechanical stress of central fat accumulation, and the underlying blood vessels show through the transparent skin. Striae are typically wide (>1 cm), purple-red (unlike the white stretch marks of pregnancy or weight gain), and found on the abdomen, flanks, thighs, breasts, and upper arms.
Easy bruising (ecchymosis) results from both dermal thinning and increased capillary fragility — minor pressure, even from routine palpation, can produce bruising.
Clinical importance for MT: this is not ordinary thin skin. Standard massage pressure that would be unremarkable in a healthy client can tear Cushing skin. Friction techniques, aggressive stretching, tape application, and even firm palpation can cause tissue damage. The therapist must recalibrate their entire pressure scale downward.

Why Osteoporosis Develops

Cortisol inhibits osteoblast activity (bone formation) while simultaneously stimulating osteoclast activity (bone resorption). It also reduces intestinal calcium absorption and increases renal calcium excretion — creating a triple assault on bone density.
The resulting osteoporosis is often severe and develops more rapidly than postmenopausal osteoporosis. Vertebral compression fractures are common (30–50% of Cushing patients) and can occur from minimal stress — sitting down abruptly, coughing, or sneezing.
Trabecular bone (vertebral bodies, ribs, pelvis) is affected more than cortical bone because trabecular bone has a higher surface area-to-volume ratio and higher turnover rate.
Renal calculi (kidney stones) may develop from the excess calcium mobilized from bones and excreted by the kidneys.

Immune Suppression

Cortisol suppresses virtually every component of the immune response: reduces lymphocyte and eosinophil counts, inhibits cytokine production, suppresses antibody synthesis, and impairs macrophage function.
Cushing patients are significantly immunocompromised — they are susceptible to opportunistic infections, and their inflammatory response to existing infections may be blunted (masked infections that progress without typical signs of inflammation).

Cardiovascular and Metabolic Consequences

Cortisol has mineralocorticoid activity at high levels — it promotes sodium and water retention, producing hypertension (80% of Cushing patients) and peripheral edema
Cortisol-driven gluconeogenesis and peripheral insulin resistance produce hyperglycemia — diabetes mellitus develops in approximately 20% and glucose intolerance in up to 80%
Dyslipidemia accelerates atherosclerosis

Signs and Symptoms

Characteristic Body Habitus

Moon face: rounded, plethoric (red) facial appearance with fat deposition in the cheeks and temporal fossae; hirsutism (excessive facial hair in women) from adrenal androgen excess
Buffalo hump: cervicodorsal fat pad over C7–T2; drives forward head posture
Truncal obesity with thin extremities: pendulous abdomen with spindly arms and legs ("apple on sticks" body habitus) — central fat accumulation + peripheral muscle wasting and fat loss
Supraclavicular fat pads: fullness above the clavicles

Integumentary

Parchment-thin, fragile skin — translucent, easily torn
Wide purple-red striae on abdomen, flanks, thighs, breasts, and upper arms (>1 cm width distinguishes from common stretch marks)
Easy bruising from minimal trauma — may appear spontaneously
Poor wound healing from combined immunosuppression and collagen deficit
Hirsutism and acne (from adrenal androgen excess)

Musculoskeletal

Proximal muscle weakness and wasting — difficulty climbing stairs, rising from chairs, lifting overhead; visible wasting of deltoids, quadriceps, gluteals
Osteoporosis with pathological fracture risk — vertebral compression fractures (back pain, height loss, kyphosis), rib fractures, hip fractures from minimal trauma
Back pain — often the presenting complaint, from vertebral compression fractures or paraspinal muscle strain under altered posture
Peripheral edema — from mineralocorticoid effects of excess cortisol

Neuropsychiatric

Emotional lability — rapid swings from euphoria to depression
Depression (50–80% prevalence), anxiety, insomnia
Cognitive dysfunction — poor concentration and memory
Psychosis in severe cases

Cardiovascular

Hypertension (80% of patients)
Hyperglycemia (fasting glucose elevated; frank diabetes in 20%)

Assessment Profile

This Assessment Profile evaluates the musculoskeletal, integumentary, and postural effects of hypercortisolism. The MT's role is to identify the tissue vulnerabilities that govern treatment safety — skin fragility, bone fragility, muscle wasting, and immune compromise — and to modify every aspect of treatment accordingly.

Subjective Presentation

Chief complaint: Client typically presents for back pain (from vertebral compression fractures or postural strain), generalized weakness ("I can't do the things I used to — stairs are hard, lifting is hard"), or stress/anxiety management. Most have a known diagnosis — either iatrogenic (on long-term prednisone) or endogenous (post-surgical or under treatment). The body habitus changes are often the client's primary psychological concern.
Pain quality: Back pain from compression fractures is acute, sharp, and localized to the fracture site; postural strain pain is dull, aching, and bilateral in the thoracolumbar junction; muscle weakness is described as heaviness and fatigue rather than pain; generalized achiness from edema and metabolic derangement.
Onset: Iatrogenic — symptoms develop gradually over months of steroid use; client can often identify when the body changes began relative to starting medication. Endogenous — insidious onset over months to years.
Aggravating factors: Any physical exertion requiring proximal strength; prolonged sitting or standing worsens back pain; jarring movements or sudden trunk loading risk fracture; cold environments worsen edema; stress amplifies emotional lability.
Easing factors: Rest reduces muscle fatigue; supported sitting reduces back pain; medical management (surgical removal of tumor; steroid tapering when possible) reverses symptoms over months.
Red flags: Acute severe back pain with or without minimal trauma → suspect vertebral compression fracture; medical referral before treatment. Signs of adrenal crisis (if steroids have been abruptly discontinued: severe fatigue, hypotension, nausea, confusion) → emergency referral; do not treat. New neurological symptoms (limb weakness, bowel/bladder changes) with back pain → suspect spinal cord compression from pathological fracture; emergency referral.

Observation

Local inspection: Moon face with facial plethora and hirsutism; buffalo hump (cervicodorsal fat pad); truncal obesity with pendulous abdomen; thin extremities with visible proximal muscle wasting (deltoid hollowing, quadriceps thinning); wide purple-red striae on abdomen, flanks, and thighs; spontaneous bruising; skin appears thin and translucent; peripheral edema (ankles, hands); supraclavicular fullness. Acne on face and upper back. If the client is post-surgical or in remission, these features may be resolving but residual.
Posture: Forward head posture driven by cervicothoracic fat pad weight; increased thoracic kyphosis; increased lumbar lordosis compensating for anterior weight shift and pendulous abdomen; rounded protracted shoulders from pectoral shortening secondary to kyphosis; overall S-curve exaggeration. Height loss if vertebral compression fractures have occurred.
Gait: May show cautious gait pattern from fracture fear and proximal weakness; difficulty rising from seated (may push up with arms — Gower's-like compensation); widened base of support for stability; slow and deliberate.

Palpation

Tone: Proximal muscles (deltoids, quadriceps, gluteals) are soft, atrophied, and lacking normal resting tone — this is catabolic wasting, not relaxation. Paraspinal muscles may be hypertonic as they compensate for altered posture and vertebral instability. Upper trapezius and cervical muscles may be hypertonic from the forward head posture driven by the buffalo hump.
Tenderness: Point tenderness over specific spinous processes (especially T7–T12) may indicate vertebral compression fracture — do not apply pressure to these areas; refer for imaging. Generalized low-grade tenderness in proximal muscles reflecting the catabolic state. Rib tenderness on palpation may indicate rib fracture — cease rib palpation if point tenderness is found; refer for imaging. Skin may bruise from palpation pressure that would be innocuous in a healthy client.
Temperature: Skin is typically warm from cortisol-driven vasodilation; edematous areas may feel cool. No characteristic temperature asymmetry pattern.
Tissue quality: Skin fragility is the dominant palpation finding. Skin is parchment-thin, translucent — subcutaneous vessels may be visible. Tissue tears and bruises under pressure that would be unremarkable in normal skin. Striae feel depressed and inelastic. Subcutaneous tissue over the trunk is padded (fat deposits) while extremity tissue feels thin and bony with little subcutaneous cushion. The buffalo hump fat pad feels dense and rubbery — it is not a muscle or bony prominence; it is a discrete fat deposit that does not respond to massage. Edematous areas pit with gentle pressure.

Motion Assessment

AROM: Proximal weakness dominates — shoulder abduction and flexion are effortful; hip flexion from seated is weak; trunk extension may be painful or limited if compression fractures are present. Cervical ROM may be restricted by the buffalo hump mass limiting extension and rotation. Trunk flexion may provoke pain at compression fracture sites. Overall ROM reflects weakness and postural alteration rather than joint restriction.
PROM / end-feel: PROM exceeds AROM in shoulder and hip (muscular weakness, not capsular restriction). End-feel is normal tissue stretch unless compression fracture guarding produces a protective/empty end-feel at the trunk. Do not force trunk ROM if compression fracture is suspected — empty end-feel with pain before anatomical limit = stop.
Resisted testing: Proximal weakness pattern — reduced strength in shoulder abduction, hip flexion, knee extension; grip strength reduced. Painless weakness (catabolic, not inflammatory). Non-myotomal distribution. Testing should use gentle resistance only — the weakened muscles cannot tolerate standard manual resistance testing.

Special Test Cluster

The Cushing SOT cluster screens for the tissue vulnerabilities that determine treatment safety — skin integrity, bone integrity, proximal strength, and postural derangement. Direct confirmation of Cushing syndrome is a medical diagnosis (24-hour urine cortisol, dexamethasone suppression test).

Test	Positive Finding	Purpose
Skin Integrity Assessment (CMTO)	Parchment-thin skin; visible subcutaneous vessels; spontaneous bruising; wide purple-red striae >1 cm; skin turgor reduced	Screen tissue fragility to determine safe pressure limits; positive findings mandate significant pressure reduction across all techniques
Vertebral Percussion/Palpation Screen (CMTO)	Point tenderness over specific spinous processes (T7–T12 most common) on gentle palpation or percussion	Screen for vertebral compression fracture; positive finding = do not treat the area; medical referral for imaging
Proximal Muscle Strength Screen (CMTO)	Inability to maintain shoulder abduction against gentle resistance; difficulty rising from seated without arm push-off	Confirm proximal myopathy; quantifies functional limitation; establishes baseline for monitoring
Postural Assessment (supplementary)	Forward head, increased thoracic kyphosis with cervicodorsal fat pad, increased lumbar lordosis, protracted shoulders, height loss	Document postural derangement from fat redistribution and vertebral fractures; guides positioning and treatment focus
Blood Pressure and Heart Rate (supplementary)	Hypertension (>140/90 mmHg); tachycardia if anxious or in adrenal crisis	Screen cardiovascular safety; hypertension is present in 80% — may require treatment modifications for position changes

Conditional cluster — if back pain is acute or new: Add rib spring test (very gentle) and trunk compression test to screen for rib and vertebral fractures. Apply these tests with extreme caution — minimal force only. Any point tenderness or acute pain reproduction = stop testing, refer for imaging. In Cushing syndrome, fractures occur from forces that would be trivial in a healthy skeleton.

Differential Assessment

Condition	Key Distinguishing Feature
Metabolic syndrome / simple obesity	Central obesity overlap, but metabolic syndrome lacks purple striae (>1 cm, purple-red), proximal muscle wasting, skin fragility, buffalo hump, and moon face; no cortisol elevation
Addison disease (adrenal insufficiency)	The functional opposite — cortisol deficiency produces hypotension, hyperpigmentation, weight loss, fatigue, and hypoglycemia; no central obesity or moon face
Hypothyroidism	Weight gain and fatigue overlap, but hypothyroidism produces myxedema (non-pitting), cold intolerance, bradycardia, and delayed DTRs; no purple striae or muscle wasting
Polycystic ovary syndrome (PCOS)	Hirsutism, acne, and central obesity overlap in women, but PCOS lacks skin fragility, purple striae, proximal myopathy, and buffalo hump; PCOS has menstrual irregularity and androgen elevation without cortisol excess
Steroid myopathy without full Cushing	Proximal weakness overlap in patients on lower steroid doses, but without the full constellation of body habitus changes; may represent early or mild Cushing — medical re-evaluation warranted

CMTO Exam Relevance

CMTO Appendix category A3 (systemic/endocrine conditions)
Iatrogenic cause is the #1 tested concept — always ask about long-term corticosteroid use in intake; this is by far the most common cause of Cushing syndrome encountered in clinical practice
Skin fragility and fracture risk are the two primary safety concepts tested — know that standard massage pressure may tear skin or fracture bones in these clients
Addison disease is the functional opposite (cortisol deficiency vs. cortisol excess) — comparing the two conditions is a common exam question
The visual identification triad (moon face, buffalo hump, truncal obesity with thin limbs) with purple striae is the classic exam presentation
Know that abrupt steroid discontinuation causes adrenal crisis — massage therapists should never advise stopping or reducing corticosteroids
Immune suppression means the therapist must be healthy and the treatment environment must be clean — this is a standard exam safety expectation
Approximately 20% have diabetes mellitus comorbidity — cross-reference with diabetes-mellitus for hypoglycemia protocols

Massage Therapy Considerations

Primary therapeutic target: stress and anxiety management within the extreme physical limitations imposed by tissue fragility; secondary targets include postural compensation from fat redistribution, proximal muscle deconditioning, and pain from vertebral compression fractures — all addressed with dramatically modified pressure and technique
Sequencing logic: begin with the safest, gentlest possible contact to assess real-time tissue response before progressing; establish that the skin can tolerate the lubricant and the lightest touch before attempting any therapeutic technique. Address postural tension (cervical, upper thoracic) with light techniques after tissue safety is confirmed. Never progress to deep or vigorous work — the tissue cannot tolerate it.
Safety / contraindications: skin fragility is the overriding safety concern — parchment-thin skin tears under pressure that would be innocuous in a healthy client; use ample lubricant, extremely light pressure, and broad contact surfaces (palms, not fingertips or elbows); no friction techniques, no cross-fiber work, no tape; monitor for bruising during the session. Osteoporosis with pathological fracture risk — no deep pressure over the spine, ribs, or pelvis; no joint mobilization involving thrust or Grade III–IV forces; no vigorous stretching; extreme care with position changes and table transfers. Immune suppression — the therapist must be healthy (no active infections, cold sores, respiratory illness); clean linens and sanitized treatment room. Avoid treatment if the client has signs of active infection (which may be masked by immunosuppression).
Heat/cold guidance: warm applications are generally tolerable and may provide comfort for muscle aching and stiffness — use tepid to warm (not hot) moist towels; monitor skin closely for burns (thin skin is more vulnerable to thermal injury). Cold applications should be used cautiously (thin skin, fragile capillaries). No vigorous contrast hydrotherapy.

Treatment Plan Foundation

Clinical Goals

Provide stress and anxiety reduction through parasympathetic activation within safe pressure limits
Address postural muscle tension (cervical, upper thoracic) from forward head posture and cervicothoracic fat pad loading
Support proximal muscle function through gentle circulatory techniques (maintenance, not strengthening)
Monitor tissue integrity throughout — the absence of skin damage during a session is itself a clinical goal

Position

Side-lying is often the most comfortable and safest position — accommodates the pendulous abdomen, reduces rib compression, and allows access to back and extremities without prone positioning on fragile anterior skin
Supine with semi-reclined positioning for anterior work — bolster under the knees; avoid flat supine if abdominal weight produces respiratory discomfort
Prone with extreme caution only — the pendulous abdomen may be uncomfortable; breast pressure on thin skin is a concern; use a body cushion system or pregnancy pillow if prone is attempted; many Cushing clients are best treated entirely in side-lying and supine
Table transfers require assistance — proximal weakness makes independent mounting/dismounting difficult; position changes must be slow and supported to avoid falls and fracture risk from jarring movements
Use ample padding and soft linens — thin skin over bony prominences (elbows, knees, sacrum) is vulnerable to pressure damage

Session Sequence

Gentle holding and light effleurage to the upper back in side-lying — establish contact; assess skin response to lubricant and lightest touch; observe for immediate bruising or skin irritation; if skin tolerates, proceed
Light effleurage and very gentle petrissage to upper trapezius and cervical musculature — address the forward head posture tension driven by the buffalo hump; use broad palmar contact; do not use thumb or elbow pressure; do not attempt to mobilize or reduce the buffalo hump — it is a fat deposit, not a muscular or fascial restriction
Light effleurage to the thoracolumbar paraspinals — avoid direct pressure over spinous processes (fracture risk); stay lateral on the erector spinae mass; assess for point tenderness that would suggest compression fracture
Gentle upper extremity work — light effleurage to the wasted proximal muscles (deltoids, triceps, biceps); the goal is circulatory support to catabolic tissue; do not use deep techniques — there is insufficient muscle mass and the overlying skin is fragile
Gentle lower extremity work in supine — light effleurage to thighs and legs; avoid pressure over areas with visible bruising or striae; if peripheral edema is present, gentle centripetal effleurage may be used if the edema is from cortisol mineralocorticoid effects (not cardiac or renal in origin — confirm)
Gentle hand and foot work — broad palmar contact; calming technique to close the session; monitor skin integrity throughout
Reassessment — inspect skin for any new bruising, redness, or damage that occurred during the session; document any skin changes; note subjective relaxation and anxiety reduction

Adjunct Modalities

Hydrotherapy: tepid to warm (not hot) moist towel application to upper back and cervical area before manual work — improves comfort; monitor skin closely — thin skin burns more easily than normal skin at lower temperatures; test temperature on a less-affected area first. No vigorous contrast hydrotherapy. No cold packs directly on skin (use multiple layers of insulation).
Remedial exercise (on-table): gentle diaphragmatic breathing to facilitate parasympathetic response — this may be the most valuable on-table intervention given the limitations on manual work; gentle active cervical ROM (rotation, lateral flexion) within pain-free range to maintain mobility around the buffalo hump; no resistive exercises (muscles are catabolic and bones are fragile).

Exam Station Notes

Demonstrate extreme pressure modification — the examiner expects to see visibly lighter pressure than for any other client population; verbalize why ("This client's skin and bones are fragile from long-term cortisol exposure — I'm using broad contact and light pressure to avoid tissue damage")
Demonstrate skin assessment before, during, and after treatment — verbalize that you are monitoring for bruising and skin tears
Demonstrate awareness of fracture risk — verbalize avoidance of spinous process pressure and aggressive positioning ("I'm avoiding direct pressure on the spine because Cushing syndrome causes significant osteoporosis with fracture risk from minimal stress")
Ask about steroid medications during intake — the examiner expects medication awareness in any client presenting with cushingoid features

Verbal Notes

Pressure negotiation: "Because your condition affects your skin and bones, I'm going to use very gentle techniques today. Your skin is more delicate than usual and your bones may be more fragile, so I'll be keeping the pressure light and using broad, flat contact with my hands. If at any point anything feels uncomfortable — even a little — tell me immediately."
Positioning assistance: "I'd like to help you get on and off the table today. With the muscle weakness, I want to make sure you're safe and comfortable. I'll guide you through the position changes so there's no sudden movement."
Bruising awareness: "It's possible you may notice some light bruising after the session even with gentle pressure — that's related to your condition affecting the skin and blood vessels. If you notice anything significant, let me know at your next appointment."
Infection awareness: "I want you to know that I'm only working with you today because I'm feeling completely healthy. If I ever have any sign of illness — even a mild cold — I'll reschedule our session, because your immune system is working differently right now."

Self-Care

Gentle daily walking (15–20 minutes) to maintain proximal muscle function and bone stress within safe limits — walking is weight-bearing enough to provide skeletal stimulus without excessive fracture risk; avoid high-impact activities
Skin protection: moisturize daily to maintain skin integrity; wear long sleeves to protect fragile skin from minor trauma; avoid adhesive bandages or tape directly on skin when possible
Fall prevention: remove trip hazards at home; install grab bars in the bathroom; wear non-slip footwear — the combination of proximal weakness, osteoporosis, and altered balance makes falls especially dangerous
Calcium and vitamin D supplementation as directed by physician — bone protection is critical; do not advise supplements independently (medication interactions with steroids are complex)

Key Takeaways

Cushing syndrome is most commonly iatrogenic from long-term corticosteroids — always audit medication history; any patient on chronic prednisone or equivalent is at risk
Skin is parchment-thin and tears under standard massage pressure — use extreme caution, broad contact, ample lubricant, and dramatically reduced pressure; friction techniques are contraindicated
Osteoporosis with pathological fracture risk means no deep pressure over spine, ribs, or pelvis; no vigorous mobilization; no trunk flexion loading; vertebral compression fractures occur from minimal stress
Proximal muscle wasting (painless, Type II fiber catabolism) produces the characteristic "apple on sticks" habitus — thin extremities with central fat accumulation
The buffalo hump (cervicodorsal fat pad) drives forward head posture and increased thoracic kyphosis — it is a fat deposit, not a treatment target; do not attempt to mobilize or reduce it
Immune suppression is clinically significant — the therapist must be healthy; the treatment environment must be clean; be aware that infections in the client may present without typical inflammatory signs
Addison disease is the functional opposite (cortisol deficiency) — comparing the two is a standard exam topic
Abrupt steroid discontinuation can precipitate adrenal crisis — never advise stopping or reducing corticosteroid medications