INTERESTING CASE OF BACK ACHE

DR.ANIRUDH J SHETTY PROF.DR.G.ELANGOVAN’S UNIT

24 year old female came with the complaints of

pain in the lower back radiating to the right lower limb -5 days

Patient was apparently normal 5 days back when she developed severe pain which radiated from the lower back uptill the right malleoli .

Pain was sharp,constant,stabbing,electric shock like pain which was distributed in the region below the right buttock .Aggravated on walking ,change in posture,sneezing

Patient specifically c/o of the pain in the lumbosacral region.

Patient also c/o not being able to appreciate hot or cold water on the lateral side of right feet or feel her clothing

h/o urge incontinence + h/o bowel incontinence +

No h/o headache ,vomiting,blurring of vision No h/o any cranial nerve involvement No h/o fever or night sweats No h/o involvement or weakness of the

upper limb No h/o seizures No h/o trauma

No h/o any involuntary movements

Past h/o – not a k/c/o DM/HTN/Tb/Seizure disorderPersonal h/o - attained menarche at 14 yrs h/o menorrhagia +

O/E – Pt conscious oriented afebrile hydration fair severe pallor(+) no icterus,clubbing,cyanosis,LAN sternal tenderness+

B.P – 110/70 mmHg

P.R – 88/min

JVP not elevated

CNS – Higher mental functions – normal UL – Tone n power (N)

LL - RT LT

BULK N N

TONE DECREASED N

RT LT POWER HIP 4- 5 KNEE 4- 5 ANKLE 4- 5 EHL WEAK N

DTR RT LT

KNEE + ++ ANKLE ABSENT + BICEPS ++ ++ TRICEPS ++ ++

SUPERFICIAL REFLEXES

CORNEAL REFLEX – (+) CONJUCTIVAL REFLEX – (+) ANAL REFLEX- ABSENT PLANTAR R L MUTE FLEXOR

CRANIAL NERVES – NORMAL

SENSORY SYSTEM LOSS OF ALL MODALITIES OF SENSATION

OVER LATERAL ASPECT OF RT FOOT LOSS OF SENSATION OVER THE PERIANAL

REGION

AUTONOMIC INVOLVEMENT

URGE INCONTINENCE +

BOWEL INCONTINENCE +

NO CEREBELLAR SIGNS

NO MENINGEAL SIGNS

CVS – S1S2 + No murmurs RS – NVBS + no added sounds P/A – Soft hepatomegaly + no spleenomegaly

IMPRESSION : COMPRESSIVE TYPE OF MYELORADICULOPATHY

MOTOR LEVEL : L1 SENSORY LEVEL:BELOW L-5 REFLEX LEVEL : L-5 AUTONOMIC INVOLVEMENT : S2,3,4

2 PACKED CELLS T.TRAMADOL INJ.RANTAC INJ CEFTRIAXONE I.V FLUIDS T.PARA

TREATMENT

INVESTIGATIONS

CBC Hb-4.2 TC-17000 DC-P22,L76,E2 PLATLET-30000

RFT RBS-96 UREA - 26 CREAT-0.6

SODIUM- 140 K+ -4.2

LFT T.B-0.8 D.B-0.2 SAP-88 SGOT- 30

SGPT-40 ALBUMIN-4gm

ECG- WNL CHEST X RAY- WNL

USG ABDOMEN LIVER SPAN-15.2 CM SPLEEN- 12.1 CM

RBC’S :severe microcytic hypochromic RBC’s

Anisopoikilocytosis seen.few target cells seen

WBC’S : Leukocytosis observed. Lymphocyte predominence more than 10% blasts seen.

PLATLETS: Severe thrombocytopenia seen.

IMPRESSION: To r/o acute leukemia

P/S STUDY

PREVERTEBRAL AND PARAVERTEBRAL SOFT TISSUE LESIONS WITH INTRASPINAL EXTENSION AT D-11,D-12,L5 TO S3

VERTEBRAL LEVEL. S/0 METASTATIC DEPOSITS

MRI REPORT

Hb-6.2 PCV- 25% TC-25,000 DC-BLAST 80%

?AML

Haematology GH

Hypercellular marrow Abnormal premyelocytes and myelocytes

seen. Myeloblast 40% Vacoulated blast (+) Erythroid progenitors reduced Occasional megakayocytes seen.

Impression – AML Type 4 with dysplasia

BONE MARROW REPORT

2 PACKED CELLS 2 PLATLETS CYTOSINE ARBINOSIDE 150 mg od 7 days ADRIAMYCIN 30 mg od 3 days ETOPOSIDE 100mg od 3 days INJ DEXA 8 mg iv bd Inj Tramadol 1gm iv hs

RADIOTHERAPY – Total dose of 180cGY in 10 fractions

TREATMENT

Compression of the spinal cord from

metastatic cancer located outside the spinal

cord,subarachnoid space and duramater.

METASTATIC EPIDURAL SPINAL CORD COMPRESSION

Metastatic epidural spinal cord compression (MESCC) is a devastating complication of cancer .

It is estimated to develop in approximately 5% to 14% of all cancer patients.

Although most patients with MESCC have limited survival, up to one third will survive beyond 1 year.

METASTATIC EPIDURAL SPINAL CORD COMPRESSION

If left untreated, virtually 100% of these patients would become paraplegic; therefore, it is considered a true medical emergency and immediate intervention is required.

Thus, it is essential to consider aggressive therapy to preserve or improve the quality of life and prevent paraplegia.

Physically, MESCC occurs in one of three ways:

(1) continued growth and expansion of vertebral bone metastasis into the epidural space. (2) destruction of vertebral cortical bone, causing vertebral body collapse with displacement of bony fragments into the epidural space.

(3) neural foramina extension into the epidural space by a paraspinal mass.

PATHOPHYSIOLOGY

Although multifactorial, the most significant damage caused by MESCC appears to be vascular in nature.

The epidural tumor causes epidural venous plexus compression, which leads to

spinal cord edema. The increased vascular permeability and edema lead to increased

pressure on the small arterioles. Capillary blood flow diminishes as the disease progresses, leading to white matter ischemia. Prolonged ischemia eventually results in infarction and permanent cord damage.

Back pain is the most common presenting symptom (88% to96%)

weakness (76% to 86%),

sensory deficits (51% to 80%)

autonomic dysfunction (40% to 64%)

CLINICAL PRESENTATION

The most common level of the MESCC involvement is :

thoracic spine (59% to 78%),

lumbar (16% to 33%)

cervical spine (4% to 15%)

Breast cancer(29 %) Lung cancer (17%) Prostate cancer(14%) Sarcomas Melanomas Lymphoma and leukemia

TUMOURS CAUSING MESCC

MRI is the standard modality for imaging of the central nervous system in cancer

patients. It has a very high sensitivity (93%), specificity (97%), and accuracy

(95%) in diagnosing MESCC Since patients can have synchronous,

multifocal MESCC, an MRI of the entire spine should be performed promptly in

anyone suspected of having MESCC

DIAGNOSIS

In terms of predicting ambulatory outcome, one of the most important factors is the rapidity of symptom onset. Other important prognostic factors

include radiosensitive histology (eg, multiple myeloma, germ-cell tumors, lymphomas,

and small-cell carcinoma) and pretherapy ambulatory function.

PROGNOSIS

CORTICOSTEROIDS Corticosteroids must be started as soon as

possible in anyone suspected of having MESCC even before radiographic diagnosis,

because they can be discontinued rapidly with a negative diagnosis. They decrease cord edema, and they serve as an effective bridge to definitive

therapy

THERAPY

Based on several studies, an IV loading dose of 10 mg dexamethasone followed

by a maintenance dose of 4 to 6 mg (IV or orally) every 6 to 8 hours should be sufficient for most patients.

Furthermore, patients should be started on a proton-pump inhibitor for GI prophylaxis.

Palliative radiotherapy has long been the standard of care in the treatment of patients

with MESCC.

Although multiple fractionation schedules have been reported in the literature, a total of 30 Gy in 10 fractions is the one most

frequently employed

RADIOTHERAPY

back pain relief maintenance of ambulation bladder function improvement

Motor function improvement

Upfront chemotherapy (with a planned

consolidative radiation) may be

considered in select, newly diagnosed

patients with excellent neurological status

and very chemosensitive tumors

Radiation alone has been the standard treatment for MESCC, although results

with radiation alone are disappointing. There are several reasons for this:

SURGERY

(1) some tumors (eg, renal cell, sarcoma, and melanoma) are not radiosensitive;

(2) even in radiosensitive tumors, it may take several days to deliver a radiation dose large enough to cause a response during which time the spinal cord damage may continue

(3) the most commonly used radiation dose and schedule (30 Gy in 10 fractions) is

insufficient to provide long-term local control of gross tumor (except for

radiosensitive tumors), so tumor may regrow

to cause a recurrence of MESCC even after initial clinical response

For years laminectomy and postoperative radiotherapy were frequently combined.

Recently, many have advocated the use of direct decompressive and maximal-

debulking surgery with intraoperative stabilization of the spine (in appropriate

cases) followed by postoperative radiation therapy

Recently, many have advocated the use of direct decompressive and maximal-

debulking surgery with intraoperative stabilization of the spine (in appropriate cases) followed by postoperative radiation therapy. Since over 85% of

spinal metastases arise anterior to the spinal cord, direct attempts at anterior

spinal decompression seems logical.

The advantages of direct decompressive surgery include removal of the tumor with

a resultant decrease in tumor burden that allows for more effective postoperative

radiotherapy. immediate relief of the cord compression

and immediate stabilization of the spinal column, which can be achieved

by the same operation.

THANK YOU