INICET Orthopedics Previous Year Questions (2018–2026)

The correct answer is Physiological conduction block.

Neurapraxia is the mildest peripheral nerve injury in Seddon's classification. It is a temporary physiological conduction block, usually from focal demyelination or ischemia, with the axon and all connective-tissue sheaths intact. Because there is no axonal disruption, there is no Wallerian degeneration and recovery is complete (days to weeks). In contrast, axonotmesis involves axonal discontinuity with intact sheaths, and neurotmesis is complete nerve-trunk transection.

Incorrect Options:

• Axonal discontinuity: defines axonotmesis (axon disrupted, sheaths preserved), with Wallerian degeneration and slower recovery - not neurapraxia.
• Nerve trunk damage: describes neurotmesis (complete transection of the nerve), the most severe injury needing surgery.
• Endoneurium disruption: corresponds to higher-grade injury (Sunderland grade 3+), not the conduction block of neurapraxia.

High-Yield Facts:

• Neurapraxia = conduction block, axon intact, full recovery (best prognosis).
• Axonotmesis = axon disrupted, sheaths intact, Wallerian degeneration occurs.
• Neurotmesis = complete transection, worst prognosis, needs surgical repair.
• Seddon's 3 grades map to Sunderland's 5 grades.

Figure: Seddon's classification - neurapraxia (conduction block, axon intact), axonotmesis (axon disrupted, sheaths intact), and neurotmesis (complete transection).

The correct answer is Fasciotomy.

Acute compartment syndrome is a surgical emergency. Rising intracompartmental pressure exceeds capillary perfusion pressure, causing ischemia; a measured pressure of 90 mmHg (far above the ~30 mmHg threshold / delta pressure under 30 mmHg) plus pain out of proportion to analgesia mandates immediate decompression by emergency fasciotomy. The newly absent pulse is a late, ominous sign of advanced ischemia - it should never be awaited and makes urgent fasciotomy even more critical to salvage the limb and prevent Volkmann ischemic contracture and rhabdomyolysis. Conservative measures or discharge would risk irreversible muscle/nerve necrosis.

Incorrect Options:

• Hot fomentation: increases vasodilation/edema and does nothing to relieve the raised compartment pressure; it wastes critical time.
• Cold fomentation: causes vasoconstriction that can worsen ischemia and does not decompress the compartment.
• Reassurance and send home: dangerous - delay leads to irreversible muscle necrosis, contracture, and limb loss.

High-Yield Facts:

• ACS is a surgical emergency treated by urgent fasciotomy.
• Fasciotomy if compartment pressure >30 mmHg or delta pressure under 30 mmHg.
• Earliest/most reliable sign is pain on passive stretch.
• Pulselessness is a LATE sign - never wait for it.

Figure: Leg fasciotomy - a long longitudinal incision releases the fascial compartment to relieve pressure, later covered by a skin graft.

The correct answer is Osteomalacia.

Bone pain with proximal muscle weakness (proximal myopathy) plus the biochemical panel of normal calcium, low phosphate, high ALP, and high PTH is the classic picture of osteomalacia, usually from vitamin D deficiency. Vitamin D deficiency reduces calcium absorption, which drives a secondary rise in PTH that keeps serum calcium normal but causes phosphaturia (low phosphate); defective osteoid mineralization raises ALP. The secondary hyperparathyroidism is the mechanism, but the disease producing this patient's bone pain and myopathy is osteomalacia. X-rays may show Looser zones (pseudofractures).

Incorrect Options:

• Primary hyperparathyroidism: calcium would be HIGH (with low phosphate, high PTH); here calcium is normal, so it is excluded.
• Paget disease: shows very high ALP but NORMAL calcium, phosphate, and PTH - not low phosphate with high PTH.
• Hyperparathyroidism secondary to vitamin D deficiency: this is the underlying mechanism, not the clinical diagnosis; the syndrome of bone pain + proximal myopathy with this panel is termed osteomalacia.

High-Yield Facts:

• Osteomalacia panel: Ca normal/low, PO4 low, ALP high, PTH high.
• Proximal myopathy + bone pain are hallmark clinical features.
• X-ray shows Looser zones (pseudofractures).
• Primary hyperPTH has HIGH calcium; normal calcium here rules it out.

Figure: Osteomalacia - softened, demineralized bone with bowing deformity and a pseudofracture (Looser zone, arrows).