What It Means

Grading of Hypoxemia (by PaO₂):

Clinical Significance of PaO₂ < 50 mmHg

1. Cellular hypoxia — tissues and organs receive critically insufficient oxygen, threatening organ function.
2. Sympathetic stimulation — early signs include restlessness, agitation, tachycardia, and dysrhythmias. If prolonged, this gives way to progressive acidosis and circulatory depression.
3. Cerebral blood flow increases — the brain attempts to compensate by dramatically increasing cerebral blood flow when PaO₂ drops below 50 mmHg.
4. Late signs (indicating decompensation): obtundation, bradycardia, hypotension, and eventually cardiac arrest.
5. Cyanosis may not be clinically visible if the patient is also anemic.

Key Distinction: Hypoxemia vs. Hypoxia

• Hypoxemia = low oxygen in the blood (measured by PaO₂ or SpO₂)
• Hypoxia = inadequate oxygen delivery to the tissues

Clinical Action

• Supplemental oxygen (high-flow)
• Identification and treatment of the underlying cause (e.g., pneumonia, ARDS, pulmonary embolism, pneumothorax, severe asthma)
• Possible non-invasive or invasive mechanical ventilation

Acute Kidney Injury (AKI) — Treatment

Modern terminology uses AKI (Acute Kidney Injury) rather than "acute renal failure," as it captures the full spectrum from mild to severe dysfunction. AKI is defined as a rapid decline in GFR over hours to days, causing retention of urea/creatinine and dysregulation of fluid, electrolytes, and acid-base balance. — Brenner and Rector's The Kidney

I. General Principles

II. Treatment by AKI Type

A. Prerenal AKI (Most Common)

• Cause: Reduced renal perfusion (dehydration, hemorrhage, heart failure, sepsis)
• Treatment:
  • Restore circulating blood volume with isotonic balanced crystalloids (preferred over normal saline, which increases major adverse kidney events)
  • Red blood cell transfusion for hemorrhagic hypovolemia
  • Avoid hydroxyethyl starch colloids (associated with increased need for RRT)
  • For heart failure: inotropes, afterload reduction, mechanical cardiac assist as needed
  • For hepatorenal syndrome: IV albumin + terlipressin (vasopressin analogue) or norepinephrine + octreotide + midodrine; definitive treatment = liver transplantation

B. Intrinsic AKI (e.g., Acute Tubular Injury)

• No specific proven pharmacologic therapy for ATN — supportive care is the mainstay
• Glomerulonephritis/Vasculitis: immunosuppressive agents, anticomplement therapy, or plasmapheresis
• Allergic interstitial nephritis: stop offending drug; glucocorticoids may help if AKI persists
• Scleroderma renal crisis: ACE inhibitors
• Thrombotic thrombocytopenic purpura (TTP): urgent plasma exchange
• Atypical HUS: complement blockade (e.g., eculizumab)
• Rhabdomyolysis: aggressive IV fluids (up to 10 L/day); consider alkaline diuresis (sodium bicarbonate in 0.45% saline) to prevent cast formation; diuretics if urine output < 200–300 mL/hr despite adequate fluid loading

C. Postrenal AKI (Obstruction)

• Prompt relief of obstruction is key:
  • Urethral obstruction: transurethral or suprapubic catheter
  • Ureteric obstruction: percutaneous nephrostomy or ureteral stent
• Relief is usually followed by a post-obstructive diuresis lasting several days — monitor and replace fluids/electrolytes

III. Management of Metabolic Complications

IV. Nutrition in AKI

V. Renal Replacement Therapy (RRT)

• Refractory hyperkalemia
• Severe metabolic acidosis
• Refractory volume overload
• Uremic symptoms (encephalopathy, pericarditis, bleeding)

VI. Drug Dosing

AKI Treatment — Summary

General Priorities

1. Optimize hemodynamics — restore perfusion (MAP > 65 mmHg)
2. Remove all nephrotoxins (NSAIDs, ACE-i, ARBs, aminoglycosides)
3. Treat the underlying cause
4. Manage metabolic complications
5. Initiate RRT when indicated

By AKI Type

Metabolic Complications

Nutrition

• 20–30 kcal/kg/day, enteral route preferred
• Protein: 0.8–1.0 g/kg/day (non-dialysis) → up to 1.7 g/kg/day (on CRRT)

Renal Replacement Therapy (RRT)

Corrective Osteotomy — Overview & Indications

Definition

Indications

Pre-Operative Evaluation

Clinical

• Full history of original injury, prior surgeries, hardware
• Manual stress of the malunion site (pain = possible nonunion, not malunion)
• Neurovascular exam
• Range of motion of joints proximal and distal to the deformity
• Identify compensatory joint deformities — these must also be addressed, or the limb will remain disabled despite a corrected bone

Radiographic

• AP and lateral radiographs including proximal and distal joints
• Bilateral 51-inch standing alignment films for lower extremity deformity
• Identify and measure:
  • Mechanical and anatomic axes
  • Joint orientation angles (see table below)
  • Center of Rotation of Angulation (CORA) — the key landmark for planning correction

Key Joint Orientation Angles (Normal Values)

Types of Deformity Corrected

1. Angulation

• Characterized by magnitude and direction of the apex
• Pure frontal/sagittal plane deformities are straightforward; oblique-plane deformities (where both AP and lateral views show angulation at the same level) require special planning
• Key tool: CORA (Center of Rotation of Angulation) — the point where the proximal and distal bone axes intersect; osteotomy at the CORA produces correction without translation

2. Rotation

• Requires osteotomy + rotational realignment
• Level of deformity often not obvious — muscle/tendon pull and neurovascular anatomy guide osteotomy placement
• Most isolated rotational deformities corrected with a transverse osteotomy

3. Translation

• Three correction strategies:
  1. Single transverse osteotomy — pure translation without angulation
  2. Single oblique osteotomy at the deformity level — corrects alignment and gains length
  3. Two opposing wedge osteotomies — treats translation as two equal, opposite angulations

4. Length (Shortening/Overdistraction)

• Measured from joint center to joint center vs. contralateral limb
• May require lengthening osteotomy with distraction osteogenesis (Ilizarov technique)

5. Combined Deformities

• Each deformity type is characterized independently
• Not all deformities may require correction — small sagittal translations may be functionally insignificant
• Correction order and method planned systematically before surgery

Types of Osteotomy

Fixation After Osteotomy

• Internal fixation: plates, screws, or intramedullary nails — for acute corrections
• External fixation: for gradual correction, limb lengthening, infected cases, or complex multiplanar deformities (e.g., Taylor Spatial Frame)

Common Clinical Examples

• High Tibial Osteotomy (HTO): medial compartment knee OA in young, active patients — shifts load to lateral compartment
• Distal femoral osteotomy: lateral compartment OA with valgus knee
• Calcaneal osteotomy: flatfoot (adult-acquired), hindfoot valgus
• Metatarsal osteotomy: hallux valgus correction
• Pelvic/periacetabular osteotomy: hip dysplasia

Osteoclasis vs. Osteotomy

Key Points

1. Osteotomy = open, controlled, surgical bone cut — the standard for most deformity corrections.
2. Osteoclasis = closed, forceful fracture of bone — used in specific contexts:
   • In distraction osteogenesis (Ilizarov method): a low-energy osteoclasis of only the posterior cortex after cutting the anterior cortices produces a corticotomy that maximally preserves the periosteum, leading to superior bone regeneration.
   • In spinal surgery: SPO performed through an ankylosed disc space uses osteoclasis to open the anterior column, but this is increasingly avoided due to risks of great vessel injury (aorta/vena cava) and creation of an anterior column void.
3. The fundamental difference is control and invasiveness: osteotomy gives the surgeon precise control over the bone cut; osteoclasis exploits the bone's natural fracture line through applied force with minimal soft tissue disruption.