Pelvic Axis, Pelvic Diameters, and Key Points for Labour

What the Page Covers

1. The obstetric/pelvic axis
2. Pelvic diameters and their clinical relevance
3. Points to ponder - key exam/clinical facts

1. Pelvic Axis (Curve of Carus / Obstetric Axis)

• It is obtained by joining the axes of the inlet, pelvic cavity, and outlet - creating a J-shaped curve
• The direction of movement changes at the level of the ischial spines: the head moves downward and backward first, then shifts to downward and forward
• The curve has convexity fitting the sacral curvature (i.e., it curves anteriorly, following the concavity of the sacrum)
• It is also called the "curve of Carus" after the anatomist Karl Gustav Carus

2. Pelvic Diameters

"Pelvic diameters vary from one patient to the other just as the height and weight. During labour the absolute size of the pelvis is not significant, but the size relative to the foetal head is vital."

3. Points to Ponder (Exam Focus)

Point 1: Obstetric Conjugate

"Obstetric conjugate is the antero-posterior diameter which the foetus must negotiate while descending, hence important."

• Panel A: Fetal head above the pelvic inlet - occiput above ischial spines (not yet engaged)
• Panel B: Biparietal diameter has descended below the inlet (obstetric conjugate) - occiput at or below ischial spines = engaged

Point 2: Head Engages in the Oblique Diameter

"The head (presenting part) commonly engages in oblique diameters at the pelvic inlet."

• The ala of the sacrum restricts the posterolateral dimension
• Engaging obliquely allows the occiput to rotate anteriorly as it descends (internal rotation)

Point 3: Plane of Least Dimensions = Most Arrests

"Plane of least dimensions (at mid-pelvis) is the plane where most cases of arrest in labour occur."

• The lower border of the pubic symphysis anteriorly
• The ischial spines laterally (interspinous diameter ~10 cm)
• The tip of the sacrum posteriorly

Summary of Clinical Relevance

• Pfenninger and Fowler's Procedures for Primary Care, p. 6678 (engagement and obstetric conjugate)

• 55-year-old female + ringing (tinnitus) in right ear x 6 months
• AC > BC in right ear = Positive Rinne = sensorineural hearing loss (or normal hearing)
• ABC (Absolute Bone Conduction) normal = Schwabach test normal = cochlear/inner ear function matches examiner = confirms the hearing loss is NOT due to cochlear damage OR the cochlea is intact
• Wait - if ABC is normal, that means bone conduction is intact/normal, and since AC > BC (positive Rinne), this is consistent with normal hearing in the right ear
• Tinnitus with normal hearing tests in a 55-year-old female = Tinnitus as the primary complaint, possibly early sensorineural or functional tinnitus

10-Mark Exam Answer

Clinical Case Interpretation

DIAGNOSIS: Subjective Tinnitus (Right Ear)

• AC > BC (Positive Rinne): Air conduction is better than bone conduction in the right ear. This is the normal physiological finding (AC is normally ~30 dB better than BC). It rules out a conductive hearing loss in the right ear.
• ABC normal: The Schwabach test compares the patient's bone conduction with that of a normal-hearing examiner. A normal ABC means the patient's cochlear (inner ear) function is intact and equal to normal. This rules out significant sensorineural hearing loss.

EXPLANATION OF THE CONDITION (According to Modern Understanding)

Definition

Classification

Modern Pathophysiology

1. Peripheral trigger: Subclinical cochlear hair cell damage (often at high frequencies, not yet detectable on tuning fork tests) causes reduced input to the auditory nerve
2. Central gain increase: The central auditory cortex, deprived of normal input, upregulates its own spontaneous firing rate - a process called maladaptive neuroplasticity
3. Phantom sound perception: This aberrant, increased spontaneous neural activity is interpreted by the brain as sound - the "ringing" the patient hears
4. Limbic system involvement: In chronic tinnitus, the limbic system (emotional processing) and prefrontal cortex become involved, leading to distress, sleep disturbance, and anxiety

Common Causes in This Age Group (55-year-old female)

Why ABC is Normal

• The cochlear damage is subclinical (affecting only the basal turn, high frequencies not tested by standard 512 Hz tuning fork)
• The tinnitus is central in origin rather than purely cochlear

Investigations to Order

1. Pure Tone Audiometry (PTA) - gold standard; may show high-frequency dip at 4000 Hz (noise notch) or sloping loss
2. Tympanometry - to rule out middle ear pathology
3. Speech Discrimination Score - to assess neural involvement
4. MRI Brain with contrast (internal acoustic meatus) - mandatory for unilateral tinnitus to exclude acoustic neuroma
5. Otoacoustic Emissions (OAE) - tests outer hair cell function; may be abnormal even when audiogram appears normal

Management (Modern)

1. Counseling and reassurance - most important first step; explain the benign nature
2. Sound therapy - white noise generators/maskers reduce central gain
3. Cognitive Behavioral Therapy (CBT) - best evidence-based treatment for chronic tinnitus distress
4. Tinnitus Retraining Therapy (TRT) - combines sound therapy + counseling; aims for habituation
5. Treat underlying cause - control hypertension, stop ototoxic drugs, hearing aids if SNHL present
6. Drug therapy (limited evidence) - melatonin for sleep, antidepressants for depression comorbidity

Tuning Fork Summary Table (High-Yield for Exam)

• AC > BC = Positive Rinne = rules out conductive loss
• Normal ABC = intact cochlear function = rules out SNHL
• Unilateral tinnitus in any adult must be investigated to exclude acoustic neuroma (MRI IAM)
• Modern pathophysiology = central maladaptive neuroplasticity, not just a cochlear problem
• Best treatment evidence = CBT + TRT (not drugs)

TINNITUS - Full 10-Mark Exam Answer

Definition

• Affects up to 50 million adults in the USA; ~10% of adults have clinically significant tinnitus
• Only ~20% find it bothersome enough to seek treatment
• ~28% of acute tinnitus (< 6 months) resolves spontaneously

Classification

1. Subjective vs. Objective

2. Pulsatile vs. Non-Pulsatile

3. Primary vs. Secondary

• Primary tinnitus: No identifiable underlying cause; may or may not be associated with SNHL
• Secondary tinnitus: Due to a specific identifiable cause (outside of SNHL)

Most common type in clinical practice: Subjective, non-pulsatile, primary tinnitus - accounts for ~90% of all tinnitus referrals

Etiology / Causes

Pathophysiology (Modern Understanding)

• Sleep disturbance
• Concentration difficulty
• Anxiety and depression
• Reduced quality of life

This is why psychological treatment (CBT) is more effective than any drug for bothersome tinnitus.

Clinical Features

• Ringing, buzzing, hissing, roaring, or clanging sounds
• Quality gives a clue to cause:
  • Roaring/hissing = otosclerosis
  • Fluctuating, variable quality = Meniere's disease
  • High-pitched ringing = auditory nerve lesion (acoustic neuroma)
  • Low-pitched = Meniere's (early)
  • Pulsatile = vascular cause
• Associated symptoms: hearing loss, vertigo, aural fullness, otalgia
• Red flags (need urgent investigation):
  • Unilateral tinnitus persisting > 6 months
  • Associated asymmetric SNHL
  • Pulsatile tinnitus
  • Focal neurological signs

Investigations

Management

Step 1: Treat the Cause (Secondary Tinnitus)

• Remove cerumen - may immediately resolve tinnitus
• Stop ototoxic drugs
• Control hypertension
• Treat middle ear infection/otosclerosis
• Surgical excision if glomus tumor

Step 2: Patient Education and Reassurance

• Explain the benign nature of primary tinnitus
• Explain the central pathophysiology
• Counsel that tinnitus often habituates over time
• This alone significantly reduces distress

Step 3: Sound Therapy

• White noise maskers/sound generators - reduce central gain by providing ambient input
• Hearing aids (if SNHL present) - amplify ambient sound, effectively masking tinnitus
• Recorded masking sounds (rainfall, white noise) for sleep

Step 4: Psychological Therapies (Best Evidence)

Step 5: Pharmacotherapy (Limited Role)

• No medications are approved for tinnitus in the USA or Europe
• Benzodiazepines (diazepam 2-5 mg TDS) - temporary symptomatic relief only
• Tricyclic antidepressants (amitriptyline 25-75 mg HS) - for associated depression/sleep
• Melatonin - for sleep disturbance
• Note: No drug has been shown to cure tinnitus

Step 6: Emerging/Invasive Options (Severe, Refractory)

• Transcranial magnetic stimulation (TMS) - modulates auditory cortex activity
• Cochlear implants - for profound SNHL with tinnitus; often dramatically reduces tinnitus
• Transtympanic corticosteroids - for sudden SNHL-associated tinnitus

Summary (High-Yield Points for Exam)

COMPARE & CONTRAST: Adhimantha (Ayurvedic) vs. Primary Open Angle Glaucoma & Primary Angle Closure Glaucoma

I. Introduction

II. Ayurvedic Concept of Adhimantha

Dosha Involvement

Pathogenesis (Samprapti) - Ayurvedic View

• Vitiated doshas travel upward via siras (blood vessels/channels) to the head and eyes
• They obstruct the srotas (channels) supplying the eye
• This leads to increased pressure within the eye (Abhishyanda = conjunctival congestion + increased fluid)
• Results in damage to Dristi (the optic disc/visual capacity)
• Progressive destruction of Dristi = blindness

The Ayurvedic concept of obstruction of srotas causing pressure build-up is analogous to impaired aqueous outflow causing raised IOP

Clinical Features (Ayurvedic Description)

• Severe, unbearable pain in the eye (Shirashool, Akshi Shool)
• Redness of the eye
• Watering, photophobia
• Colored halos around lights (Indradhanush darshan = rainbow vision)
• Diminution of vision
• Headache and nausea (in acute types)
• Stony hard eye on palpation
• In chronic types - gradual painless visual loss

Prognosis (Ayurvedic)

Treatment (Ayurvedic)

• Snehana (oleation) with medicated oils (Triphala ghrita, Jeevantyadi ghrita)
• Swedana (sudation/fomentation)
• Virechana (therapeutic purgation) - to eliminate vitiated Pitta
• Nasya (nasal instillation of medicated oils) - to relieve Vata in head
• Netra Tarpana (eye bathing with medicated ghee)
• Lekhana (scraping treatment)
• Siravedha (bloodletting from periocular veins) - corresponds to reducing venous congestion
• Systemic Ayurvedic medicines: Triphala, Saptamrita Lauha

III. Modern Concept: Primary Open Angle Glaucoma (POAG)

Definition

• Retinal nerve fibre layer (RNFL) thinning
• Glaucomatous optic nerve damage (cupping)
• Characteristic visual field loss
• Open anterior chamber angle on gonioscopy
• IOP is an important modifiable risk factor (Normal IOP = 10-21 mmHg)

Pathogenesis

1. Mechanical - raised IOP deforms the lamina cribrosa, directly damaging retinal nerve fibers as they exit the optic nerve head
2. Ischaemic - compression of blood vessels supplying the optic nerve head leads to ischaemic damage

Risk Factors

• Raised IOP (>21 mmHg) - most important modifiable risk factor
• Age (> 40 years)
• Family history (4x risk in siblings)
• Black race (4x more common, earlier onset)
• Myopia
• Diabetes mellitus, systemic vascular disease

Clinical Features

• Asymptomatic until late - the "silent thief of sight"
• No pain, no redness (differentiates from PACG)
• Peripheral visual field loss initially (arcuate scotoma, nasal step)
• Tunnel vision in advanced disease
• IOP may be elevated (but can be normal - Normal Tension Glaucoma)
• Cup-to-Disc (C:D) ratio > 0.5, asymmetry >0.2

Investigations

Treatment

• Topical IOP-lowering drops (first line):
  • Prostaglandin analogues (latanoprost, bimatoprost) - increase uveoscleral outflow
  • Beta-blockers (timolol) - decrease aqueous production
  • CAIs (dorzolamide), alpha-2 agonists (brimonidine)
• Laser: Selective Laser Trabeculoplasty (SLT) - increases trabecular outflow
• Surgery: Trabeculectomy with Mitomycin C when medical treatment fails

IV. Modern Concept: Primary Angle Closure Glaucoma (PACG)

Definition

PACG may account for up to 50% of all glaucoma globally and is more prevalent in Asians. It progresses rapidly and causes more blindness than POAG.

Mechanism

• Aqueous cannot flow freely from posterior to anterior chamber through the pupil
• Pressure builds in the posterior chamber
• Peripheral iris bows forward (iris bombé)
• Iris contacts the trabecular meshwork, blocking aqueous outflow
• IOP rises suddenly and markedly (50-80 mmHg in acute attack)

Risk Factors

• Female sex (more commonly affected)
• Age > 60 years
• Hypermetropia (short, small eye with shallow anterior chamber)
• Short axial length, thick lens
• Asian and Indian ethnicity
• Family history

Clinical Features (Acute Attack - APAC)

Chronic PACG

• Insidious, progressive, like POAG
• Angle closes silently with peripheral anterior synechiae (PAS)
• Visual field loss similar to POAG
• Often bilateral

Treatment

V. Comparison Table: Adhimantha vs. POAG vs. PACG

VI. Correlation Summary

Key Points to Remember (Exam Focus)

1. Adhimantha = glaucoma in Ayurveda; described as severe churning pain with vision loss
2. POAG = chronic, painless, open angle - "silent thief of sight"
3. PACG = painful, red eye, raised IOP, closed angle - requires emergency treatment
4. Both cause optic nerve damage - Ayurveda calls this Dristi kshaya
5. Ayurvedic concept of blocked srotas = modern concept of impaired aqueous outflow
6. LPI (Laser Peripheral Iridotomy) is the cornerstone of PACG treatment
7. Prostaglandin analogues are first-line for POAG
8. PACG is more common in Asian women, hypermetropes, short axial length
9. POAG is more common in Black populations, myopes, elderly
10. Sannipata Adhimantha (all doshas) = Asadhya = corresponds to absolute/end-stage glaucoma