THIS IS AN ONLINE E LOG BOOK TO DISCUSS OUR PATIENT'S DE-IDENTIFIED HEALTH DATA SHARED AFTER TAKING HIS SIGNED INFORMED CONSENT. HERE WE DISCUSS OUR PATIENT'S PROBLEMS THROUGH SERIES OF INPUTS FROM AVAILABLE GLOBAL ONLINE COMMUNITY EXPERTS WITH AN AIM TO SOLVE THOSE PATIENT'S CLINICAL PROBLEMS WITH COLLECTIVE CURRENT BEST EVIDENCE BASED INPUTS.
EMR SUMMARY:
Age/Gender: 70 Years/Male
Address:
Discharge Type: Relieved
Admission Date: 29/08/2025 01:31 PM
Diagnosis
UREMIC ENCEPHALOPATHY
SEPSIS SECONDARY TO LEFT LOWER LIMB CELLULITIS
ACUTE ON CHRONIC CKD
K/C/O HTN SINCE 1 YEAR
Case History and Clinical Findings
CHIEF COMPLAINTS: FEVER SINCE 4 DAYS, NECK PAIN SINCE 4 DAYS, LEFT LOWER LIMB
SWELLING SINCE 3 DAYS
HISTORY OF PRESENTING ILLNESS: PATIENT WAS APPARENTLY ASYMPTOMATIC 3 DAYS
BACK THEN HE DEVELOPED LEFT LOWER LIMB SWELLING WHICH WAS INTERMITTENT AND RELIEVED ON MEDICATION. H/O FEVER SINCE 4 DAYS WHICH WAS HIGH GRADE,
INSIDIOUS IN ONSET, ASSOCIATED WITH CHILLS AND RIGOR. NECK PAIN INSIDIOUS IN
ONSET, AGGREVATED ON MOVEMENT, ASSOCIATED WITH RIGIDITY. LEFT LOWER LIMB
SWELLING EXTENDING ENTIRELY UPTO THE KNEE, RAISED LOCAL TEMPERATURE AND
PAIN. NO COMPLAINTS OF VOMITINGS, CHEST PAIN OR PALPITATIONS.
PAST HISTORY: K/C/O HTN SINCE 1 YEAR (ON AMLODIPINE 5 MG). N/K/C/O DM, CVA, CAD, TB, ASTHMA OR EPILEPSY.
PERSONAL HISTORY: MARRIED, MIXED DIET, NORMAL APPETITE, REGULAR BOWEL AND BLADDER HABITS, NO KNOWN ALLERGIES, REGULAR ALCOHOL CONSUMPTION PRESENT.
GENERAL EXAMINATION: PATIENT IS C/C/C. NO PALLOR, ICTERUS, CYANOSIS, CLUBBING, LYMPHADENOPATHY OR PEDAL EDEMA.
VITALS: TEMP-AFEBRILE, BP-90/60 MMHG, PR-115,
RR- 30CPM, SPO2- 96% AT RA, GRBS-222 MG/DL. GCS: E4V5M6
SYSTEMIC EXAMINATION: CVS, CNS, RS, P/A- NORMAL
** Tentative Date Page-2
KIMS HOSPITALS
Investigation
COMPLETE URINE EXAMINATION (CUE) 29-08-2025 02:52:PM COLOUR Pale
yellow APPEARANCE Clear REACTIONAcidicSP.GRAVITY1.010ALBUMIN Trace SUGAR Nil BILE SALTS Nil BILE PIGMENTS Nil PUS CELLS2-4EPITHELIAL CELLS2-3RED BLOOD
CELLS Nil CRYSTALS Nil CASTS Nil AMORPHOUS DEPOSITS Absent OTHERS Nil Arterial Blood Gas
Analysis (ABG) 30-08-2025 11:15:PM PH7.30PCO230.0PO259.0HCO314.6St.HCO316.1BEB-
10.3BEecf-10.5TCO231.2O2 Sat90.4O2 Count11.5RFT 30-08-2025 11:15:PM UREA71
mg/dlCREATININE2.8 mg/dl URIC ACID5.3 mmol/LCALCIUM8.3 mg/dlPHOSPHOROUS2.7
mg/dlSODIUM140 mmol/LPOTASSIUM3.3 mmol/L.CHLORIDE 98 mmol/L
RFT 02-09-2025 01:44:AM
UREA53 mg/dl CREATININE2.3 mg/dl URIC ACID4.6 mmol/LCALCIUM7.8 mg/dlPHOSPHOROUS2.0
mg/dlSODIUM139 mmol/LPOTASSIUM3.4 mmol/L.CHLORIDE98 mmol/L
HEMOGRAM: HB-10.9 G/DL, TLC-20500, RBC- 3.2 MILLIONS/MM3, PLT- 1.6 LAKH/MM3, APTT-32s, PT-16s, INR-1.11, LDH-283 IU/L, ESR-85MM/1ST HR, BLOOD LACTATE-3.4.
USG IMPRESSION: GRADE-III RPD CHANGES OF RIGHT KIDNEY, GRADE-I RPD CHANGES OF LEFT KIDNEY, B/L RENAL CORTICAL CYSTS.
Treatment Given (Enter only Generic Name)
IV FLUIDS NS@ 75ML/HR
INJ. PIPTAZ 2.25 GM IV/TID
INJ. CLINDAMYCIN 600MG IV/BD
INJ. PAN 40MG IV/OD
INJ. NEOMAL 1 GM IV/SOS IF TEMPERATURE >101F
INJ. THIAMINE 200MG IV/TID
TAB. DOLO 650MG IV/TID
NEB. IPRAVENT 6TH HRLY AND BUDECORT 8TH HRLY
LEFT LOWER LIMB ELEVATION AND REGULAR DRESSINGS
SYP. POTKLOR 15 ML PO/TID
TAB. CHYMORAL FORTE PO/TID
Advice at Discharge
SALT RESTRICTION <2GM/DAY
FLUID RESTRICTION <1.5LIT/DAY
TAB.CLINDAMYCIN 600MG PO/TID 7 DAYS
TAB.AGUMENTIN 625MG PO/TID 7 DAYS
TAB. PAN 40MG PO/OD FOR 7 DAYS
TAB. DOLO 650MG PO/SOS
TAB. CHYMORAL FORTE PO/TID FOR 5 DAYS
** Tentative Date Page-3
KIMS HOSPITALS
TAB.NODOSIS 500MG PO/BD FOR 1MONTH
TAB.OROFER XT PO/OD FOR 1 MONTH
TAB. SHELCAL PO/OD FOR 1MONTH
REGULAR DRESSINGS FOR LEFT LOWER LIMB
Follow Up
REVIEW TO NEPHROLOGY OPD AFTER 1 WEEKS/SOS WITH RFT AND HEMOGRAM REPORTS
REVIEW TO GENERAL SURGERY OPD FOR REGULAR DRESSINGS
When to Obtain Urgent Care
IN CASE OF ANY EMERGENCY IMMEDIATELY CONTACT YOUR CONSULTANT DOCTOR OR
ATTEND EMERGENCY DEPARTMENT.
Preventive Care
AVOID SELF MEDICATION WITHOUT DOCTORS ADVICE, DONOT MISS MEDICATIONS. In case of Emergency or to speak to your treating FACULTY or For Appointments, Please Contact:
08682279999 For Treatment Enquiries Patient/Attendant Declaration : - The medicines prescribed
and the advice regarding preventive aspects of care, when and how to obtain urgent care have been
explained to me in my own language
SIGNATURE OF PATIENT /ATTENDER
SIGNATURE OF PG/INTERNEE
SIGNATURE OF ADMINISTRATOR
SIGNATURE OF FACULTY
Discharge Date
Date:3/9/2025
Ward: AMC
NEPHROLOGY
[05-09-2025 21:02] PPM 1: The main point of interest in this patient was the diagnostic uncertainty where OPLL due to Narketpally fluorosis was confounding a diagnostic uncertainty between neck rigidity and meningitis vs uremia sepsis encephalopathy similar to the illustrative case published in @PPM7 @PPM6@PPM5 @PPM2 @CR @PPM3's report here: https://pubmed.ncbi.nlm.nih.gov/40674544/
While that case was mentioned in passing in the above report mainly to illustrate the Narketpally imaginary pillow sign, it was archived in detail and can be accessed from the reference 29 of the paper here: https://onlinelibrary.wiley.com/doi/10.1111/jep.70186
[06-09-2025 01:06] PPM 3: Certainly! I will analyze the diagnostic challenges involving OPLL from Narketpally fluorosis confounded with meningitis vs. uremic sepsis encephalopathy. The main contents of the report are as follows:
- *Introduction and clinical background*: Overview of the complex diagnostic scenario and key clinical features.
- *Fluorosis and OPLL*: Explains the relationship between fluorosis and OPLL, including diagnostic methods.
- *Meningitis vs. meningism*: Differentiates between true meningitis and OPLL-induced meningism.
- *Uremic sepsis encephalopathy*: Details pathophysiology and diagnostic features of USAE.
- *Diagnostic approach*: Provides a systematic method for differential diagnosis.
- *Management strategies*: Outlines targeted treatment approaches for each condition.
- *Conclusion*: Summarizes key points for clinical differentiation.
-------
# Diagnostic Complexity in Ossification of Posterior Longitudinal Ligament (OPLL) with Fluorosis: Differentiating Neck Rigidity of Meningitis versus Uremic Sepsis Encephalopathy
## 1 Introduction and Clinical Background
The *diagnostic challenge* presented in this case represents a fascinating convergence of musculoskeletal, infectious, metabolic, and neurological pathologies. This complex clinical scenario involves a patient with *ossification of the posterior longitudinal ligament (OPLL)* in the context of *endemic fluorosis* from the Narketpally region, which creates diagnostic uncertainty between meningeal signs suggestive of meningitis and altered mental status potentially attributable to *uremic sepsis encephalopathy*. The mention of the "Narketpally imaginary pillow sign" references a specific clinical observation documented in previous case reports from this region known for its high fluoride content in groundwater. This sign reportedly manifests as a characteristic posture adopted by patients to alleviate discomfort from cervical spine pathology related to fluorosis.
The complexity of this case lies in the fact that *neck rigidity—a classic sign of meningeal irritation—can also present in advanced cervical OPLL due to mechanical constraints on spinal movement. Simultaneously, **systemic illness* with sepsis and uremia can produce encephalopathy that further clouds the clinical picture. This intersection of pathologies creates a diagnostic dilemma requiring careful consideration of epidemiology, clinical presentation, diagnostic findings, and targeted investigations to arrive at an accurate diagnosis and appropriate treatment plan. The following sections will systematically analyze each component of this complex presentation and provide a framework for differential diagnosis.
## 2 Understanding Fluorosis and OPLL in the Narketpally Context
### 2.1 Epidemiological and Pathophysiological Considerations
- *Endemic fluorosis* in the Narketpally region of India results from *excessive fluoride content* in groundwater, which leads to chronic fluoride accumulation in the body. This condition affects multiple systems, with *skeletal fluorosis* being a prominent manifestation characterized by increased bone density, ligament calcification, and osteophyte formation.
- The *pathophysiological relationship* between fluorosis and OPLL is well established, with studies demonstrating that fluoride stimulates osteoblastic activity and promotes bone formation in ligamentous tissues. Research has shown that fluoride levels are significantly higher in patients with OPLL compared to controls, with urinary fluoride levels >1.6 mg/L serving as a diagnostic indicator of fluorosis.
- *Radiological characteristics* of fluorosis-associated OPLL include continuous, segmental, mixed, or focal patterns of ossification along the posterior longitudinal ligament. The continuous and mixed variants are associated with higher urinary fluoride levels and tend to produce more severe compression of the spinal canal . Advanced imaging with *CT scanning* is superior to plain radiography in characterizing the extent and pattern of OPLL, with occupying ratios >60% and hill-shaped ossification associated with poorer neurological outcomes.
### 2.2 Clinical Manifestations of OPLL in Fluorosis
- The *primary clinical presentation* of OPLL ranges from asymptomatic incidental findings to progressive neurological deficits. Myelopathic features including gait disturbance, bladder dysfunction, and sensory changes are common in advanced cases, while radicular symptoms may predominate in earlier stages .
- *Cervical rigidity* and limited range of motion are hallmark features of advanced OPLL, which can mimic meningismus. This mechanical restriction results from the ossification process itself rather than true muscular spasm associated with meningeal irritation. The aforementioned "Narketpally imaginary pillow sign" represents a compensatory posture that patients adopt to minimize discomfort and neurological symptoms through strategic head positioning.
- The *mass occupying effect* of OPLL can lead to significant spinal canal compromise, with dural penetration occurring in severe cases. The "Rule of Nine" classification system helps surgeons assess the feasibility and safety of anterior resection based on the distribution of ossification within the spinal canal.
## 3 Differentiating Meningitis from OPLL-Induced Meningism
### 3.1 Clinical Assessment of Neck Rigidity
- *True meningismus* typically presents with nuchal rigidity that is painful in all directions of movement and is often accompanied by other signs of meningeal irritation, such as Kernig's and Brudzinski's signs. In contrast, *OPLL-related restricted movement* may demonstrate directional preference, with typically greater limitation in extension than flexion, and lacks the associated meningeal signs .
- The *temporal pattern* of symptom development offers important diagnostic clues: meningeal signs in infectious meningitis typically develop acutely over hours to days, while OPLL-related restrictions develop insidiously over months to years. However, acute exacerbation of OPLL symptoms can occur following minor trauma or whiplash injuries, potentially mimicking acute meningitis presentation .
- *Systemic symptoms* such as fever, photophobia, and severe headache are characteristic of meningitis but absent in isolated OPLL. The presence of these symptoms should prompt immediate investigation for infectious or inflammatory meningeal processes.
### 3.2 Diagnostic Evaluation
- *Cerebrospinal fluid (CSF) analysis* remains the gold standard for diagnosing meningitis. In bacterial meningitis, CSF typically shows elevated opening pressure, neutrophilic pleocytosis, elevated protein, and decreased glucose levels. Viral meningitis demonstrates lymphocytic predominance with normal glucose levels. These CSF findings would be normal in cases of isolated OPLL.
- *Neuroimaging* plays a crucial role in differentiation. While both conditions might show enhancement on post-contrast imaging, meningitis typically demonstrates leptomeningeal enhancement, whereas OPLL shows characteristic ossification along the posterior longitudinal ligament on CT scans. MRI in meningitis may also show complications such as hydrocephalus, cerebral edema, or venous thrombosis, which are absent in OPLL .
- *Advanced imaging techniques* including the "K-line" assessment on neutral lateral radiographs help determine whether OPLL exceeds the line connecting the midpoints of the spinal canal at C2 and C7. K-line negative status suggests poor posterior shift of the spinal cord after laminoplasty, helping guide surgical decision-making .
Table: Differentiating Features Between Meningitis and OPLL-Induced Meningism
| *Feature* | *Meningitis* | *OPLL-Induced Meningism* |
|---------------------------|--------------------------------|-----------------------------------|
| *Onset* | Acute (hours to days) | Chronic (months to years) |
| *Fever* | Present | Absent |
| *Headache* | Severe, diffuse | Variable, often neck-centered |
| *Kernig's/Brudzinski's* | Positive | Negative |
| *CSF Findings* | Abnormal inflammatory markers | Normal |
| *Imaging* | Leptomeningeal enhancement | Ossification along PLL |
| *Systemic Symptoms* | Prominent | Absent or related to fluorosis |
## 4 Uremic Sepsis Encephalopathy (USA) – Pathophysiology and Clinical Features
### 4.1 Sepsis-Associated Encephalopathy (SAE)
- *Sepsis-associated encephalopathy* represents diffuse brain dysfunction resulting from systemic inflammatory response to infection without direct CNS infection. The pathophysiology involves *complex mechanisms* including vascular damage, endothelial activation, blood-brain barrier breakdown, altered brain signaling, brain inflammation, and apoptosis .
- The *clinical spectrum* of SAE ranges from mild symptoms such as malaise and concentration deficits to deep coma. Delirium is a common presentation, characterized by acute fluctuation in mental status, inattention, and disorganized thinking. However, SAE is not synonymous with delirium, as symptoms may bypass the delirium stage entirely .
- *Diagnostic considerations* for SAE include the presence of systemic infection meeting sepsis criteria, exclusion of other encephalopathy causes, and supportive findings on EEG (generalized theta or delta slowing) or elevated biomarkers of brain injury (neuron-specific enolase, S-100 β protein). Importantly, SAE may present in early sepsis stages before full diagnostic criteria are met .
### 4.2 Uremic Encephalopathy in the Context of Sepsis
- *Uremic encephalopathy* represents a metabolic encephalopathy resulting from accumulated toxins in renal failure. When superimposed on sepsis, the combined effect produces more profound neurological dysfunction than either condition alone. The *pathophysiological mechanisms* include blood-brain barrier disruption, neuroinflammation, neurotransmitter imbalances, and increased brain oxidative stress.
- *Clinical features* of uremic encephalopathy include cognitive impairment, memory deficits, agitation, psychosis, seizures, and various movement disorders including asterixis and myoclonus. These features help distinguish uremic encephalopathy from other encephalopathy types, though overlap exists .
- The *diagnostic approach* to uremic sepsis encephalopathy requires comprehensive assessment including renal function tests, inflammatory markers, microbiological studies, and exclusion of other metabolic derangements. Neuroimaging may show characteristic findings such as lentiform fork sign or basal ganglia changes in uremic encephalopathy, while SAE may demonstrate leukoencephalopathy or normal imaging .
## 5 Comprehensive Diagnostic Approach to the Complex Presentation
### 5.1 Systematic Evaluation Strategy
- *Initial assessment* should prioritize identifying immediately life-threatening conditions. The *ABCs (Airway, Breathing, Circulation)* take precedence, especially given the potential for sepsis-induced hemodynamic instability and neurological deterioration that might require intensive care management .
- *History gathering* should focus on establishing the temporal sequence of symptoms, particularly which developed first: neck rigidity/stiffness or altered mental status. A careful history might reveal chronic symptoms suggestive of fluorosis (dental mottling, joint stiffness, radicular symptoms) preceding acute deterioration. Epidemiological factors including residence in endemic fluorosis areas like Narketpally should be specifically queried .
- *Physical examination* must include comprehensive neurological assessment with attention to meningeal signs, focal neurological deficits, and manifestations of systemic illness. The "Narketpally imaginary pillow sign" – a characteristic posture alleviating cervical discomfort – should be specifically sought .
### 5.2 Diagnostic Investigations
- *Laboratory evaluation* should include complete blood count, comprehensive metabolic panel (assessing renal function and electrolytes), inflammatory markers (CRP, procalcitonin), urinary fluoride levels, and blood cultures. Arterial blood gas analysis helps assess metabolic derangements and acid-base status in sepsis .
- *CSF analysis* via lumbar puncture is essential when meningitis is suspected. Measurement of opening pressure, cell count with differential, glucose, protein, gram stain, culture, and appropriate PCR studies (e.g., for HSV) should be performed. CT head is recommended before LP if concern exists for
- *Neuroimaging* with *cervical spine CT* is the gold standard for characterizing OPLL extent, increased ICP or mass effect . pattern, and spinal canal compromise. MRI brain and spine helps evaluate meningeal enhancement, spinal cord compression, and alternative structural causes. The "double-layer sign" on CT suggests dural ossification, which has surgical implications .
- *Neurophysiological studies* including EEG are valuable in detecting subclinical seizures and encephalopathic patterns. Somatosensory-evoked potentials may quantify the severity of spinal cord dysfunction in OPLL.
Table: Diagnostic Findings in Key Differential Considerations
| *Test* | *OPLL with Fluorosis* | *Bacterial Meningitis* | *Uremic Sepsis Encephalopathy* |
|-------------------|--------------------------------|----------------------------------|----------------------------------|
| *Urinary Fluoride* | >1.6 mg/L | Normal | Normal or elevated |
| *CSF Analysis* | Normal | Neutrophilic pleocytosis, ↑ protein, ↓ glucose | Typically normal |
| *Cervical CT* | Ossification along PLL | Normal or mild degenerative changes | Normal or unrelated changes |
| *Renal Function*| Normal | May be abnormal in severe sepsis | Significantly abnormal |
| *Inflammatory Markers* | Normal or mildly elevated | Markedly elevated | Elevated |
| *EEG* | Normal or mild slowing | Diffuse slowing | Moderate to severe slowing |
## 6 Management Strategies for Complex Diagnostic Scenarios
### 6.1 Targeted Treatment Approaches
- *OPLL management* depends on neurological severity and radiological characteristics. *Surgical intervention* is indicated for moderate to severe myelopathy or progressive neurological deficits. Surgical options include anterior resection with or without corpectomy and fusion, posterior decompression with or without fusion, or combined approaches. The K-line status, occupying ratio, and presence of dural ossification guide surgical approach selection .
- *Fluorosis management* primarily involves *reducing fluoride exposure* by providing alternative water sources and nutritional interventions to mitigate fluoride absorption. Symptomatic management includes analgesics for bone and joint pain and physical therapy to maintain mobility .
- *Meningitis treatment* requires prompt empiric antibiotics covering likely pathogens based on patient age and risk factors, with refinement based on culture results and CSF analysis. Adjunctive corticosteroids may be beneficial in certain bacterial meningitides to reduce inflammatory complications .
- *Uremic sepsis encephalopathy management* demands a dual approach: *infection control* with appropriate antibiotics and source control, and *renal support* with volume resuscitation, correction of metabolic derangements, and renal replacement therapy when indicated. Neurological symptoms typically improve with treatment of the underlying conditions .
### 6.2 Considerations for Multidisciplinary Care
- The complexity of this presentation necessitates a *collaborative multidisciplinary approach* involving internists, neurologists, neurosurgeons, nephrologists, infectious disease specialists, and rehabilitation physicians. This team should coordinate to develop a comprehensive management plan addressing all pathological components .
- *Long-term follow-up* is essential for monitoring OPLL progression, renal function recovery, and cognitive sequelae from encephalopathy. Serial imaging may be required to assess OPLL progression, particularly if neurological symptoms worsen .
- *Rehabilitation services* including physical therapy, occupational therapy, and cognitive rehabilitation play crucial roles in functional recovery, particularly given the potential for residual neurological deficits from OPLL myelopathy and encephalopathy .
## 7 Conclusion and Key Clinical Takeaways
The diagnostic dilemma presented by this case highlights the challenges in distinguishing between OPLL-related neck rigidity, meningeal irritation, and metabolic encephalopathy in the context of endemic fluorosis and sepsis. Several key principles emerge from this analysis:
First, a *thorough history* and *physical examination* remain fundamental, with attention to epidemiological factors (e.g., residence in fluorosis-endemic areas), temporal symptom progression, and characteristic signs (e.g., the "Narketpally imaginary pillow sign").
Second, *targeted diagnostic investigations* are essential for differentiation: urinary fluoride levels and cervical spine CT for fluorosis-related OPLL; CSF analysis for meningitis; and renal function tests, inflammatory markers, and EEG for uremic sepsis encephalopathy.
Third, *simultaneous pathologies* may coexist, particularly in complex presentations. The presence of fluorosis-related OPLL does not exclude concurrent meningitis or sepsis-related encephalopathy, necessitating comprehensive evaluation.
Finally, *multidisciplinary management* is crucial for addressing the diverse pathological elements, including surgical intervention for symptomatic OPLL, infection control and renal support for uremic sepsis encephalopathy, and long-term rehabilitation for optimal functional outcomes.
This case underscores the importance of maintaining broad differential diagnosis and systematically evaluating each potential contributing condition to develop appropriate, targeted management strategies for patients with complex, multifactorial presentations.
Table: Priority Interventions Based on Diagnostic Considerations
| *Diagnostic Possibility* | *First-Line Interventions* | *Specialist Involvement Needed* |
|----------------------------|-------------------------------------------|-------------------------------------|
| *OPLL with Myelopathy* | Surgical consultation, cervical spine MRI/CT | Neurosurgery, Neurology |
| *Bacterial Meningitis* | Immediate empiric antibiotics, CSF analysis | Infectious Disease, Neurology |
| *Uremic Encephalopathy* | Renal function support, metabolic correction | Nephrology, Critical Care |
| *Sepsis-Associated Encephalopathy* | Infection source control, hemodynamic support | Infectious Disease, Critical Care |
| *Skeletal Fluorosis* | Fluoride reduction, pain management | Endocrinology, Rheumatology |
[06-09-2025 06:42] PPM 1: Thanks for these very useful insights
[06-09-2025 10:25] PPM 4: Yes, absolute feast.
[21-09-2025 19:26] PPM 1: After getting discharged from medicine on 3/9/25 as in his first EMR summary above, this patient was admitted in surgery two days later and I'm sharing that EMR summary below 👇
Age/Gender: 70 Years/Male
Address:
Discharge Type: Relieved
Admission Date: 05/09/2025 07:07 PM
Name of Treating Faculty
General Surgery
Diagnosis
LEFT LIMB CELLULITIS
Case History and Clinical Findings
C/O LEFT LOWER LIMB SWELLING SINCE 2 WEEKS
HOPI:
PATIENT WAS APPARENTLY ASYMPTOMATIC 2 WEEKS AGO THEN HE DEVELOPED LEFT
LOWER LIMB SWELLING,INSIDIOUS IN ONSET,GRADUALLY PROGRESSIVE
H/O FEVER PRESENT WITH CHILLS AND RIGORS AND RELIEVED WITH TAKING MEDICATION
NO H/O SIMILAR C/O IN THE PAST
PAST HISTORY:
K/C/O HTN SINCE 1YEARS ON REGULAR MEDICATION
K/C/O AKI UNDER DIALYSIS
K/C/O UREMIC SEPSIS 1 WEEK BACK
N/K/C/O TB, EPILEPSY, TB, ASTHMA, CVA
PERSONAL HISTORY
MARRIED, NORMAL APPETITE, VEGETARIAN, REGULAR BOWEL AND BLADDER
MOVEMENT, NORMAL MICTURITION, NO KNOWN ALLERGIES AND ADDICTIONS.
FAMILY HISTORY - NOT SIGNIFICANT
GENERAL PHYSICAL EXAMINATION:
PATIENT IS C/C/C
NO PALLOR, ICTERUS, CYANOSIS, CLUBBING OF FINGERS, GENERALISED
LYMPHADENOPATHY, EDEMA OF FEET
TEMP:99 F
Page-2
KIMS HOSPITALS
2
BP:110/80 MMHG
PR: 80 BPM
RR: 18 CPM
TEMP: 98.4 F
SP02: 99%
GRBS:120 MG/DL
SYSTEMIC EXAMINATION:
CVS: S1,S2+
RS: BAE+
CNS:NFND
LOCAL EXAMINATION:
ON INSPECTION: DIFFUSE SWELLING NOTED ON LEFT LOWER LIMB EXTENDING FROM
TOES TO BELOW KNEE LEVEL (10CM AWAY FROM BELOW KNEE)
REDDISH DISCOLOURATION ABSENT
ULCER OF IRREGULAR SHAPE PRESENT ON MEDIAL ASPECT OF LEFT LOWER LIMB
PEELING OF EPIDERMIS PRESENT WITH MILD DISCHARGE
NO LOSS OF HAIR,NO VISIBLE ENGORGED VEINS
NO VISIBLE SWELLINGS,SCARS,SINUSES
NO VISIBLE PULSATIONS
ON PALPATION:
ALL INSPECTORY FINDINGS IN TERMS OF SITE,SIZE,SHAPE,SURFACE HAVE BEEN
CONFIRMED ON PALPATION
LOCAL RAISE OF TEMPERATURE PRESENT
TENDERNESS NOT ELLICITED
PITTING EDEMA IS MINIMAL PRESENT FROM TOES TO BELOW KNEE LEVELPERIPHERAL
PULSES INTACT
RT LT
DPA ++ ++
PTA ++ ++
ATA ++ ++
PA ++ ++
NO PALPABLE INGUINAL LYMPHNODES
NO OTHER PALPABLE MASS
Page-3
KIMS HOSPITALS
Investigation
RFT 06-09-2025 08:23:AM UREA 38 mg/dl 50-17 mg/dl CREATININE 1.8 mg/dl 1.3-0.8 mg/dl URIC
ACID 5.3 mmol/L 7.2-3.5 mmol/LCALCIUM 8.9 mg/dl 10.2-8.6 mg/dl PHOSPHOROUS 4.1 mg/dl 4.5-2.5 mg/dl SODIUM 134 mmol/L 145-136 mmol/L POTASSIUM 4.9 mmol/L. 5.1-3.5mmol/L CHLORIDE 99 mmol/L 98-107 mmol/L
LIVER FUNCTION TEST (LFT) 06-09-2025 08:23:AM Total Bilurubin 1.79 mg/dl 1-0 mg/dl Direct
Bilurubin 0.69 mg/dl 0.2-0.0 mg/dl SGOT(AST) 33 IU/L 35-0 IU/L SGPT(ALT) 26 IU/L 45-0
IU/L ALKALINE PHOSPHATASE 496 IU/L 128-56 IU/L TOTAL PROTEINS 6.4 gm/dl 8.3-6.4
gm/dl ALBUMIN 2.7 gm/dl 4.6-3.2 gm/dl A/G RATIO 0.75 COMPLETE BLOOD PICTURE
(CBP) HAEMOGLOBIN 8.9 gm/dl TOTAL COUNT 11700 cells/cumm NEUTROPHILS 72% LYMPHOCYTES 20 % EOSINOPHILS 1 % MONOCYTES 7 % BASOPHILS 00 % PLATELET
COUNT 6.7 SMEAR Normocytic normochromic, PLATELETS -ADEQUATE.HEPATITIS- B
SURFACE ANTIGEN (HBSAg) RAPID TEST - Negative ANTI HCV ANTIBODIES (Rapid Test) RAPID Non
ReactivePT-16INR-1.11APTT-32.0BT-2:00MINUTESCT-4:00
MINUTES HEMOPARASITIES: NOT SEENUSG ABDOMEN AND PELVIS DONE ON
23/8/25 IMPRESSION: CHOLELITHIASIS, B/L GRADE-1 RPD CHANGESUSG CHEST WAS DONE ON 25/08/5 IMPRESSION: NO SONOLOGICAL ABNORMALITY NOTED.LIVER FUNCTION TEST
(LFT) ON 9/9/25Total Bilurubin 1.14 mg/dl Direct Bilurubin 0.28 mg/dl SGOT(AST) 19 IU/LSGPT(ALT)16 IU/L ALKALINE PHOSPHATASE 390 IU/L TOTAL PROTEINS 7 gm/dl ALBUMIN 2.60gm/dl A/G RATIO 0.59 RFT UREA 26.00 mg/dl CREATININE 1.80 mg/dl URIC ACID 4.5mmol/L CALCIUM 9.9mg/dl PHOSPHOROUS 4.2mg/dl SODIUM 137 mmol/LPOTASSIUM 5.4 mmol/LCHLORIDE 99 mmol/L
Treatment Given (Enter only Generic Name)
HIGH PROTIEN DIET
IVF NS, RL, DNS @80 ML/HR
INJ.PIPTAZ 2.25GM IV/TID
INJ.CLINDAMYVIN 400MG
INJ.PAN 40MG IV/OD
INJ.PCM 1 GM IV/SOS
T.COMBIFLAM PO/BD
T.CHYMEROL FORTE PO/TID
TAB.MVT PO/OD
TAB.VIT C PO/OD
LEFT LIMB ELEVATION
T.NODOSIS 500MG PO/BD
Page-4
KIMS HOSPITALS
T.OROFER X T PO/OD
TAB.SHELCALXT PO/OD
NEB WITH IPRATROPIYUM+BUDESONIDE 8TH FRLY
TAB.DYTOR 10MG PO/OD
Advice at Discharge
FLUID RESTRICTION<2L PER DAY
SALT RESTRICTION<1.5GM/DAY
TAB.AUGMENTIN PO/OD X7DAYS
TAB.PAN 40 MG PO/OD X7DAYS
TAB.CHYMEROL FORTE PO/OD X7DAYS
TAB.VIT C PO/OD X7DAYS
TAB.MVT PO/OD X7DAYS
TAB.COMBIFLAM X7DAYS
MUPIROCIN FOR LOCAL APPLICATION
B/L LL ELEVATION REGULARLY
Follow Up
REVIEW TO GS OPD AFTER 1 WEEK
REVIEW TO NEPHRO OPD AFTER 1 WEEK WITH RFT REPORTS
When to Obtain Urgent Care
IN CASE OF ANY EMERGENCY IMMEDIATELY CONTACT YOUR CONSULTANT DOCTOR OR ATTEND EMERGENCY DEPARTMENT.
Preventive Care
AVOID SELF MEDICATION WITHOUT DOCTORS ADVICE, DONOT MISS MEDICATIONS. In case of Emergency or to speak to your treating FACULTY or For Appointments, Please Contact:
For Treatment Enquiries Patient/Attendant Declaration: - The medicines prescribed
and the advice regarding preventive aspects of care, when and how to obtain urgent care have been
explained to me in my own language
SIGNATURE OF PATIENT /ATTENDER
SIGNATURE OF PG/INTERNEE
SIGNATURE OF ADMINISTRATOR
SIGNATURE OF FACULTY
Page-5
KIMS HOSPITALS
Discharge Date
Date:10/9/25
Ward: MSW
Unit: GS V
[21-09-2025 19.34] PPM 1: Yesterday afternoon when we examined him clinically we found an interesting additional finding that looks like a septic left knee arthritis
[21-09-2025 19:35] PPM 1: @Meta AI @PPM3 how common is septic knee arthritis spreading from lower limb cellulitis?
[21-09-2025 19:35] Meta AI: Septic knee arthritis spreading from lower limb cellulitis is not very common, but it can occur under certain conditions. Cellulitis, being a localized skin and soft tissue infection, rarely spreads directly to a joint unless there is hematogenous spread (via the bloodstream) or contiguous spread (direct extension from adjacent infected tissues). Risk factors include immunosuppression, diabetes mellitus, recent surgeries, or pre-existing joint conditions like osteoarthritis or rheumatoid arthritis. Staphylococcus aureus is the most common pathogen in such cases. Early recognition and treatment of cellulitis are critical to prevent complications like septic arthritis.¹ ² ³
Do you want to explore risk factors or management strategies further?
[21-09-2025 19:35] Meta AI: https://www.rch.org.au/clinicalguide/guideline_index/Osteomyelitis_Septic_Arthritis/
[21-09-2025 19:35] Meta AI: https://teachmesurgery.com/orthopaedic/principles/septic-arthritis/
[21-09-2025 19:35] Meta AI: https://www.orthobullets.com/trauma/1058/septic-arthritis--adult
[21-09-2025 19:50] PPM 1: Previous admission pics
[21-09-2025 19:50] PPM 1: 5/9/25 sir
[21-09-2025 20.43] PPM 3: Of course. This is an excellent and important clinical question.
The direct spread of a lower limb cellulitis into the knee joint to cause *septic arthritis is uncommon, but it is a well-recognized and serious complication.*
Here’s a detailed breakdown of the relationship, the mechanisms, and the risk factors.
### The Short Answer
While cellulitis and septic arthritis can occur simultaneously, it is *not common* for cellulitis to directly spread into the joint space to cause a septic knee. The body has robust anatomical barriers designed to prevent this. However, the same infection that causes cellulitis can indirectly lead to a septic joint through the bloodstream, or directly if those barriers are breached.
The estimated incidence of septic arthritis in the general population is 2 to 10 cases per 100,000 people per year. Only a small subset of these cases originate from a contiguous cellulitis infection.
---
### Why Direct Spread is Uncommon: The Anatomical Barrier
The knee joint is enclosed by a tough, fibrous capsule. This capsule, along with the surrounding ligaments and tissues, acts as a very effective barrier against infection. For bacteria to move directly from the skin and soft tissues of cellulitis into the joint space, they would have to invade through this capsule, which is difficult.
### How It Can Happen: The Mechanisms
Despite the barrier, septic arthritis can develop in the context of lower limb cellulitis through three primary mechanisms:
1. *Hematogenous Spread (Most Common Route):* This is the #1 way bacteria reach any joint. The initial cellulitis causes a bacteremia (bacteria entering the bloodstream). These bacteria then travel through the blood and *seed the joint. The knee, being a large, highly vascular joint, is a common target. In this case, the cellulitis is the *source of the bloodstream infection, not a direct invader.
2. *Direct Inoculation or Contiguous Spread:*
* *Traumatic Injury:* A deep wound or puncture (e.g., from a fall, a sharp object) that introduces bacteria through the skin, through the cellulitis, and directly into the joint.
* *Medical Procedures:* Infections can be introduced iatrogenically during joint aspiration, surgery, or injection if sterile technique is broken.
* *Penetrating Infection:* In severe, neglected, or rapidly progressing cellulitis, the infection can theoretically erode through the joint capsule, but this is *very rare*.
3. *Osteomyelitis:* In some cases, cellulitis can lead to infection of the adjacent bone (osteomyelitis). If the bone infection is near the joint, it can break through the bone cortex and extend into the joint space.
### Risk Factors That Increase the Likelihood
Certain conditions make it easier for a cellulitis to lead to a septic joint:
* *Pre-existing Joint Problems:* Rheumatoid arthritis, osteoarthritis, prosthetic knee joint, or previous joint surgery make the joint more susceptible to infection.
* *Immunocompromised State:* Diabetes, HIV/AIDS, chemotherapy, chronic steroid use, and advanced age weaken the immune system's ability to contain an infection.
* *Intravenous Drug Use:* Increases the risk of bacteremia and seeding in unusual sites.
* *Chronic Skin Conditions:* Conditions like chronic venous stasis ulcers or lymphedema provide a persistent portal of entry for bacteria.
### Clinical Importance: Recognizing the Red Flags
It is crucial for clinicians and patients to recognize the signs that cellulitis might be complicated by a septic joint. The symptoms of septic arthritis often *overshadow* those of cellulitis:
| Feature | Cellulitis | Septic Arthritis |
| :--- | :--- | :--- |
| *Pain* | Diffuse, aching tenderness over the skin | *Severe, intense pain* deep in the joint |
| *Swelling* | Superficial, soft, pitting edema | *Joint effusion* (fluid inside the joint), tense swelling |
| *Range of Motion* | May be limited due to pain and swelling | *Actively and passively restricted*; even slight movement is excruciating |
| *Systemic Symptoms* | Fever, chills may be present | *High fever, rigors (shaking chills), malaise* are more common |
*Key Takeaway:* If a patient with lower limb cellulitis develops a *severely painful, swollen knee that is excruciatingly painful to move*, this is a medical emergency. It must be evaluated immediately for septic arthritis, typically with joint aspiration (arthrocentesis) for fluid analysis and culture.
### Conclusion
While the *direct spread* of cellulitis into the knee joint is anatomically difficult and therefore uncommon, the presence of lower limb cellulitis *significantly increases the risk* of developing septic arthritis in the knee via *hematogenous spread* (bacteria traveling through the blood).
The overall coexistence of the two conditions is not rare, and it represents a serious clinical scenario. Any signs of deep joint pain and dysfunction in a patient with cellulitis should prompt immediate medical evaluation to rule out septic arthritis, as it is a destructive infection that requires urgent treatment.
[22-09-2025 15.10] PPM 1: Update:
Sepsis appears to have worsened today although the hemogram appears to be telling another story, which is probably not his report if you notice the dramatic exponential recovery of the hemogram in the attached trend
[22-09-2025 15.12] PPM 1: @PPM9 has noticed the progressive polyarthritis today but simply written knee, wrist, elbow without specifying that its the left knee, left elbow and right wrist as imaged here along with the wrist restriction of movement.
[22-09-2025 15:13] PPM 3: Based on the information you've provided, here is an analysis of the situation:
### 1. Data Interpretation Issue
The chart you've shared appears to be corrupted or misformatted. The test names (e.g., HD, PCV, TLC) are listed in the first column, but the numerical values in the subsequent columns do not align correctly with the headers ("Positive", "HIV:", "HBSAG - VC", "HCV - VC"). This makes it impossible to interpret the actual lab values directly from this image.
For example, a "Platelet count" of 6.0 or an "ESR" of 14.0 under a column labeled "HIV:" is illogical and indicates a formatting error, likely from copying and pasting data into a template.
### 2. Clinical Interpretation of the Update
Your update provides the crucial context. The key points are:
* *Clinical Status:* The patient's sepsis has *worsened* today. This is the primary clinical concern and is based on the patient's overall condition (e.g., fever, blood pressure, heart rate, mental status, other organ function).
* *Conflicting Data:* The hemogram (which includes tests like Hb, PCV, TLC, Platelet count) appears to show a *"dramatic exponential recovery."* This suggests the lab report shows significant improvement in blood counts, which would be unexpected and inconsistent with a worsening septic state.
* *Your Astute Observation:* You correctly suspect that *this dramatic improvement may not be accurate* for this specific patient. This is a critical red flag.
### 3. Possible Explanations for the Discrepancy
There are several likely reasons for this conflict between the clinical picture and the lab data:
1. *Sample Mix-up:* This is the most common cause of such a dramatic and clinically implausible discrepancy. The blood drawn for the lab test may have been mislabeled, or the results from another patient may have been assigned to this patient's record.
2. *Lab Error:* An error could have occurred during the analysis process within the lab instrument.
3. *Data Entry Error:* The results may have been transcribed or entered into the reporting system incorrectly.
4. *Extremely Atypical Response:* While theoretically possible, it is highly improbable that a hemogram would show dramatic improvement while the overall clinical status of sepsis is deteriorating.
### Recommended Action
Given the seriousness of sepsis, this discrepancy must be addressed immediately.
1. *Verify the Results:* *Contact the lab immediately* to verify the results and the integrity of the sample. Request a *repeaton the patient's blood sample* to confirm or rule out the reported values.
2. *Treat the Patient, Not the Paper:* *Base treatment decisions on the clinical signs of worsening sepsis.* Do not withhold necessary interventions (e.g., antibiotics, fluids, vasopressors) based on a lab report that is highly suspect and contradicts the patient's condition.
3. *Re-check Bedside Parameters:* Ensure all vital signs and clinical assessments are accurate and up-to-date.
4. *Review Trend:* If previous hemograms were available and showed severe abnormalities (e.g., very low counts), a sudden "normalization" is a strong indicator of a lab error or sample mix-up.
*In summary, trust the clinical diagnosis of worsening sepsis. The hemogram report is highly likely to be erroneous, and the most probable cause is a sample mix-up or lab error. Immediate verification is essential.*
[22-09-2025 15:16] PPM 1: @PPM9 those joint x-rays were not useful at all as we were not expecting any erosions here in what appears to be an acute septic polyarthritis.
On further history taking by @PPM10 we found he's been a regular alcoholic since he retired as a cook 10 years back and would mostly go to bed right after drinking a quarter but no other features of alcoholism beyond that. He did report knee pains developing since 1 year but not severe enough to make him take up the stick. Was on NSAIDs off and on for the knee pains
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